{"id":2423,"date":"2013-04-25T00:00:00","date_gmt":"2013-04-25T07:00:00","guid":{"rendered":"https:\/\/vermont.salk.edu\/news-release\/sunshine-hormone-vitamin-d-may-offer-hope-for-treating-liver-fibrosis\/"},"modified":"2013-04-25T00:00:00","modified_gmt":"2013-04-25T07:00:00","slug":"sunshine-hormone-vitamin-d-may-offer-hope-for-treating-liver-fibrosis","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/de\/news-release\/sunshine-hormone-vitamin-d-may-offer-hope-for-treating-liver-fibrosis\/","title":{"rendered":"Sunshine hormone, vitamin D, may offer hope for treating liver fibrosis"},"content":{"rendered":"<p>LA JOLLA, CA\u2014Liver fibrosis results from an excessive accumulation of tough, fibrous scar tissue and occurs in most types of chronic liver diseases. In industrialized countries, the main causes of liver injury leading to fibrosis include chronic hepatitis virus infection, excess alcohol consumption and, increasingly, nonalcoholic steatohepatitis (NASH).\n<\/p>\n<p>\nNow, in a new study published in the journal <em>Zelle<\/em>, scientists at the Salk Institute for Biological Studies have discovered that a synthetic form of vitamin D, calcipotriol (a drug already approved by the FDA for the treatment of psoriasis), deactivates the switch governing the fibrotic response in mouse liver cells, suggesting a potential new therapy for fibrotic diseases in humans.\n <\/p>\n<div class=\"imageCaption\"><img decoding=\"async\" alt=\"mouse liver tissue\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2013\/01\/612.jpg\"\/><\/p>\n<p>\nThis image shows mouse liver tissue with fibrosis (red), a type of scarring caused by chronic liver diseases and injuries. Salk researchers found that a drug already approved by the FDA for the treatment of psoriasis deactivates the switch governing the fibrotic response in mouse liver cells, suggesting a potential new therapy for fibrotic diseases in humans.\n<\/p>\n<p>Bilder: Mit freundlicher Genehmigung des Salk Institute for Biological Studies\n<\/p>\n<\/div>\n<p>\n&#8220;Because there are currently no effective drugs for liver fibrosis, we believe our findings would open a new door for treatment,&#8221; says senior author <a href=\"\/de\/faculty\/evans.html\/\">Ronald M. Evans<\/a>, a professor in Salk&#8217;s <a href=\"\/de\/faculty\/gene_expression_laboratory.html\/\">Genexpressionslabor<\/a> and lead researcher in the Institute&#8217;s new <a href=\"\/de\/news\/pressrelease_details.php\/?press_id=594\">Helmsley Center for Genomic Medicine<\/a>.    <\/p>\n<p>\nThe Salk study focused on a star-shaped &#8220;stellate&#8221; cell in the liver that serves as a beacon for damage. When called into action, stellate cells produce fibrotic proteins in an attempt to heal an injury. Under chronic stress, however, localized fibrosis expands, eventually leading to cirrhosis, increased risk of liver cancer, and the need for a liver transplant in advanced cases.\n <\/p>\n<p>\nThe Evans lab discovered a genetic switch through which vitamin D-related ligands such as calcitriol, a hormonally active form of the vitamin, can put the brakes on fibrosis. &#8220;Preclinical results suggest the &#8216;vitamin D brake&#8217; is highly efficacious and led us to believe that the time is right to consider a trial in the context of chronic liver disease,&#8221; says Evans, a Howard Hughes Medical Institute Investigator and holder of the March of Dimes Chair in Molecular and Developmental Biology.\n <\/p>\n<p>\nPrevious studies have shown a physiologic role for vitamin D in liver function, but &#8220;it was our discovery of high levels of vitamin D receptor (VDR) in the stellate cell that led us to consider it as a possible off switch for liver fibrosis,&#8221; says lead author Ning Ding, a research associate in the Gene Expression Laboratory.\n <\/p>\n<p>\n&#8220;Current therapeutic approaches, which treat the symptoms of liver disease, don&#8217;t stop liver fibrosis from progressing,&#8221; says Michael Downes, a senior staff scientist in the Gene Expression Laboratory and co-corresponding author on the paper. &#8220;In liver diseases where the underlying cause cannot be cured, progression to cirrhosis is currently inevitable in some people. What we have discovered is that by acting on the genome, VDR can simultaneously defend against multiple fibrotic activators. This is important because many different pro-fibrotic signaling pathways converge on the genome to affect their fibrotic response.&#8221;\n <\/p>\n<p>\nThe Salk discovery that calcipotriol counters the fibrotic response in stellate cells illuminates a potentially safer, more effective strategy capable of neutralizing multiple convergent fibrotic triggers.\n   <\/p>\n<p>\nThe Salk scientists say that clinical trials of the vitamin D analog for the treatment of liver fibrosis are being planned. The synthetic vitamin D analog is better than natural vitamin D, they say, for a couple of reasons. First, natural vitamin D, which is found in small amounts in a few foods and produced in the body by exposure to sunlight, degrades quickly, while synthetic versions of vitamin D are less susceptible to breakdown. Second, too much natural vitamin D can cause hypercalcemia, or elevated calcium in the blood, which can lead to nausea and vomiting, frequent urination, muscle weakness and joint aches and pain. The synthetic vitamin D analog, on the other hand, produces a strong response without adding calcium to the blood.\n <\/p>\n<p>\nIn addition, the researchers say this new model for treating liver fibrosis may also be helpful in treating other diseases with a fibrotic component, including those of the lung, kidney and pancreas.\n <\/p>\n<p>\nOther researchers on the study were Ruth T. Yu, Mara H. Sherman, Mathias Leblanc, Mingxiao He, Annette R. Atkins and Grant D. Barish, from the Salk Institute; Nanthakumar Subramaniam, Caroline Wilson, Renuka Rao, Sally Coulter and Christopher Liddle, of the University of Sydney (Australia); and Sue L. Lau , Christopher Scott and Jenny E. Gunton, of the Garvan Insitute for Medical Research (Australia).\n <\/p>\n<p>\nThe work was supported by grants from the <a href=\"http:\/\/www.nih.gov\/\">Nationale Gesundheitsinstitute<\/a>, der <a href=\"http:\/\/www.hhmi.org\/\">Howard Hughes Medical Institute<\/a>, der <a href=\"http:\/\/www.nhmrc.gov.au\/\">National Health and Medical Research Council of Australia<\/a>, der <a href=\"http:\/\/www.genentechfoundation.com\/\">Genentech Foundation<\/a>, der <a href=\"http:\/\/helmsleytrust.org\/\">Die gemeinn\u00fctzige Stiftung von Leona M. und Harry B. Helmsley<\/a>, der <a href=\"http:\/\/www.waxmancancer.org\/\">Samuel Waxman Krebsforschungsstiftung<\/a>, <a href=\"http:\/\/www.standup2cancer.org\/\">Stand Up to Cancer<\/a> und <a href=\"http:\/\/www.ipsen.com\/\">Ipsen\/Biomeasure<\/a>.<\/p>\n<p>For information on the commercialization of this technology, please contact Michelle Booden at 858-453-4100 x1612 or <a href=\"mailto:mbooden@salk.edu\">mbooden@salk.edu<\/a> in the Salk Office of Technology Development.<\/p>\n<p><strong><br \/>\n\u00dcber das Salk Institute for Biological Studies:<\/strong><br \/>\nDas Salk Institute for Biological Studies ist eine der weltweit f\u00fchrenden Institutionen f\u00fcr Grundlagenforschung, an der international renommierte Fakult\u00e4tsmitglieder grundlegende Fragen der Biowissenschaften in einem einzigartigen, kollaborativen und kreativen Umfeld untersuchen. Mit dem Fokus auf Entdeckungen und die Ausbildung zuk\u00fcnftiger Forschergenerationen leisten Salk-Wissenschaftler bahnbrechende Beitr\u00e4ge zu unserem Verst\u00e4ndnis von Krebs, Alterung, Alzheimer, Diabetes und Infektionskrankheiten durch die Untersuchung von Neurowissenschaften, Genetik, Zell- und Pflanzenbiologie sowie verwandten Disziplinen.\n<\/p>\n<p>\nDie Leistungen der Fakult\u00e4t wurden mit zahlreichen Auszeichnungen gew\u00fcrdigt, darunter Nobelpreise und Mitgliedschaften in der National Academy of Sciences. Das 1960 vom Polio-Impfstoff-Pionier Dr. Jonas Salk gegr\u00fcndete Institut ist eine unabh\u00e4ngige gemeinn\u00fctzige Organisation und ein architektonisches Wahrzeichen.<\/p>","protected":false},"featured_media":0,"template":"","faculty":[91],"disease-research":[],"class_list":["post-2423","disclosure","type-disclosure","status-publish","hentry","faculty-ronald-evans"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Sunshine hormone, vitamin D, may offer hope for treating liver fibrosis - Salk Institute for Biological Studies<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.salk.edu\/de\/news-release\/sunshine-hormone-vitamin-d-may-offer-hope-for-treating-liver-fibrosis\/\" \/>\n<meta property=\"og:locale\" content=\"de_DE\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Sunshine hormone, vitamin D, may offer hope for treating liver fibrosis - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"LA JOLLA, CA\u2014Liver fibrosis results from an excessive accumulation of tough, fibrous scar tissue and occurs in most types of chronic liver diseases. 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