Guest guest Posted August 24, 2009 Report Share Posted August 24, 2009 Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.sciencedaily.com/releases/2009/08/ 090823184347.htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans. The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine. "We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology. "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme. "But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung." So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said. Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market. The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow. Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis. "It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function." The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis. There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath. There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis. When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said. "So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans." Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.sciencedaily.com /releases/2009/08/090823184347.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2009 Report Share Posted August 24, 2009 MB, This is truly exciting. I said I volunteer NOW. Love and Prayers, Peggy IPF 2004, FloridaWorry looks around, Sorry looks back, Faith looks up. Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. BethModeratorFibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.sciencedaily.com/releases/2009/08/ 090823184347.htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans.The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine."We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology. "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme."But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung."So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said.Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market.The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow.Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis."It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function."The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis.There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath.There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis.When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said."So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans."Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.sciencedaily.com /releases/2009/08/090823184347.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2009 Report Share Posted August 24, 2009 Beth, I forwarded this article to my pulmodude! Thanks Z fibriotic NSIP/05 Z 65, fibriotic NSIP/05/PA And “mild†PH/10/07 No, NSIP was not self-inflicted…I never smoked! Potter, reader,carousel lover and MomMom to Darah and Sara     “I’m gonna be iron like a lion in Zionâ€Â Bob Marley Vinca Minor-periwinkle is my flower   Beth wrote:  Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article.  Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08  Web address:      http://www.sciencedaily.com/releases/2009/08/      090823184347.htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans. The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine. "We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology. "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme. "But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung." So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said. Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market. The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow. Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis. "It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function." The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis. There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath. There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis. When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said. "So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans." Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.sciencedaily.com /releases/2009/08/090823184347.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2009 Report Share Posted August 24, 2009 , Great minds think alike! I did the same thing and also to my entire family! Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 To: Breathe-Support Sent: Monday, August 24, 2009 5:35:08 PMSubject: Re: Very exciting article Beth, I forwarded this article to my pulmodude! Thanks Z 65, fibriotic NSIP/05/PA And “mild†PH/10/07 No, NSIP was not self-inflicted…I never smoked! Potter, reader,carousel lover and MomMom to Darah and Sara “I’m gonna be iron like a lion in Zion†Bob Marley Vinca Minor-periwinkle is my flower Beth wrote: Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.scienced aily.com/ releases/ 2009/08/ 090823184347. htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans. The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine. "We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology . "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme. "But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung." So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said. Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market. The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow. Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis. "It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function." The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis. There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath. There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis. When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said. "So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans." Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.scienced aily.com /releases/2009/ 08/090823184347. htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2009 Report Share Posted August 24, 2009 I am taking a copy to my Dr. on Wed.. LOL can't wait to see what see says. Love and Prayers, Peggy IPF 2004, FloridaWorry looks around, Sorry looks back, Faith looks up. , Great minds think alike! I did the same thing and also to my entire family! BethModeratorFibrotic NSIP 06/06 Dermatomyositis 11/08 From: Zion <ljz741 (AT) verizon (DOT) net>To: Breathe-Support Sent: Monday, August 24, 2009 5:35:08 PMSubject: Re: Very exciting article Beth, I forwarded this article to my pulmodude! Thanks Z 65, fibriotic NSIP/05/PA And “mild” PH/10/07 No, NSIP was not self-inflicted…I never smoked!Potter, reader,carousel lover and MomMom to Darah and Sara “I’m gonna be iron like a lion in Zion” Bob MarleyVinca Minor-periwinkle is my flower Beth wrote: Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. BethModeratorFibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.scienced aily.com/ releases/ 2009/08/ 090823184347. htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years.But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans.The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine."We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology . "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme."But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung."So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said.Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market.The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow.Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis."It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function."The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis.There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath.There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis.When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said."So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans."Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.scienced aily.com /releases/2009/ 08/090823184347. htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2009 Report Share Posted August 24, 2009 linda if you forwarded the article to your doc at penn, maybe my docs at penn will see it to Pink Joyce R (IPF 3/06) IFA 5/09 Pennsylvania Donate Life Listed 1/09 Inactive 4/09 www.transplantfund.org--- Subject: Re: Very exciting articleTo: Breathe-Support Date: Monday, August 24, 2009, 5:42 PM , Great minds think alike! I did the same thing and also to my entire family! Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 From: Zion <ljz741 (AT) verizon (DOT) net>To: Breathe-Support@ yahoogroups. comSent: Monday, August 24, 2009 5:35:08 PMSubject: Re: Very exciting article Beth, I forwarded this article to my pulmodude! Thanks Z 65, fibriotic NSIP/05/PA And “mild†PH/10/07 No, NSIP was not self-inflicted…I never smoked! Potter, reader,carousel lover and MomMom to Darah and Sara “I’m gonna be iron like a lion in Zion†Bob Marley Vinca Minor-periwinkle is my flower Beth wrote: Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.scienced aily.com/ releases/ 2009/08/ 090823184347. htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans. The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine. "We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology . "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme. "But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung." So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said. Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market. The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow. Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis. "It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function." The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis. There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath. There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis. When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said. "So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans." Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.scienced aily.com /releases/2009/ 08/090823184347. htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2009 Report Share Posted August 24, 2009  This is terribly exciting news! I am just so happy to have read this! I wonder if ther drug will come out for our use before too many of us die? This is so exciting! Joyce Rudy AZ birds Very exciting article Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.sciencedaily.com/releases/2009/08/ 090823184347.htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans. The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine. "We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology. "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme. "But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung." So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said. Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market. The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow. Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis. "It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function." The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis. There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath. There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis. When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said. "So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans." Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.sciencedaily.com /releases/2009/08/090823184347.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 25, 2009 Report Share Posted August 25, 2009 Joyce, It is very exciting research but please remember this is only research. There isn't a drug yet. They've identified the enzyme that drives the fibrotic process. Knowing that can and hopefully will lead to development of drugs and or therapies but nothing is there yet. Hopefully things will move quickly but in the meantime we keep living and taking the best care of ourselves possible. There has been so little known about how this disease happens in our bodies that a discovery like this is cause for celebration, just keep that small note of caution in there too. Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 To: Breathe-Support Sent: Monday, August 24, 2009 11:01:04 PMSubject: Re: Very exciting article  This is terribly exciting news! I am just so happy to have read this! I wonder if ther drug will come out for our use before too many of us die? This is so exciting! Joyce Rudy AZ birds Very exciting article Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.scienced aily.com/ releases/ 2009/08/ 090823184347. htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans. The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine. "We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology . "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme. "But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung." So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said. Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market. The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow. Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis. "It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function." The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis. There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath. There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis. When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said. "So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans." Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis. ScienceDaily. Retrieved August 24, 2009, from http://www.scienced aily.com /releases/2009/ 08/090823184347. htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 25, 2009 Report Share Posted August 25, 2009 This is awesome news! It gives me hope for my children who are at serious risk of developing IPF in the future. C_53_Familial IPF_5/09WashingtonTo: Breathe-Support Sent: Monday, August 24, 2009 1:28:27 PMSubject: Very exciting article Hi everyone. This article was just posted by the Pulmonary Fibrosis Foundation on Facebook. I'm copying and pasting it here as I think we all need to see this. Researchers at University of Michigan appear to have identified a specific enzyme involved in the fibrotic process. And by using therapies to attack that enzyme they are able to halt the fibrotic process. While obviously this is very early research (currently only in mice) this discovery his huge and a direction for researchers to move in. Here's the article. Beth Moderator Fibrotic NSIP 06/06 Dermatomyositis 11/08 Web address: http://www.scienced aily.com/ releases/ 2009/08/ 090823184347. htm New Therapeutic Target Could Help Patients With Pulmonary Fibrosis ScienceDaily (Aug. 23, 2009) — A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years. But researchers at the University of Michigan have discovered that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans. The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process — which involves scar-like tissue formation in an organ such as the lung. The researchers' findings will be published in the September issue of the journal Nature Medicine. "We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology . "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme. "But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung." So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said. Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market. The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow. Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis. "It remains to be seen if fibrosis is reversible," he said. "But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function." The lung disease often affects older people, Thannickal said, and its cause is generally unknown. It is possible that cumulative injuries like exposure to environmental toxins and pollutants in genetically susceptible individuals could contribute to causing fibrosis. There is a gradual scarring of the lung, thickening and contracting the organ until it loses its ability to exchange oxygen with blood, Hecker said. Patients experience extreme fatigue, rapid weight loss, chronic cough and shortness of breath. There are five million people worldwide that are affected by this disease, according to the Pulmonary Fibrosis Foundation. In the United States there are over 100,000 patients with Pulmonary Fibrosis. When U-M researchers induced the fibrotic process in the mice, they discovered that the NOX4 enzyme was elevated. By knocking down that enzyme at the genetic level or inhibiting its activity, the fibrosis was stopped, Hecker said. "So we may be able to halt lung scarring even after the injury has occurred and fibrosis is set in motion," she said. "This research provides proof of concept that we can target this pathway for therapeutic benefit, which could potentially be used in humans." Both Hecker and Thannickal left U-M this summer for the University of Alabama at Birmingham, but they plan to continue to work with Pennathur and other U-M researchers on anti-fibrotic therapies based on these studies. The patent will stay with U-M. Adapted from materials provided by University of Michigan Health System. Email or share this story: | More Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA University of Michigan Health System (2009, August 23). New Therapeutic Target Could Help Patients With Pulmonary Fibrosis.. ScienceDaily. Retrieved August 24, 2009, from http://www.scienced aily.com /releases/2009/ 08/090823184347. htm Quote Link to comment Share on other sites More sharing options...
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