COMMENTARIES
Hepatic fibrosis
Thiazolidinediones and hepatic fibrosis: don’t wait too long
Correspondence to:
Correspondence to:
Dr F Marra
Dipartimento di Medicina Interna, University of Florence, Viale Morgagni, 85, I-50134 Florence, Italy; f.marra@dmi.unifi.it
Lack of effect of delayed thiazolidinedione treatment may imply that these drugs are of limited efficacy in hepatic fibrosis, and that treatment of chronic liver disease might be successful only if the therapy were started very early
Keywords: peroxisome proliferator activated receptor gamma; hepatic fibrosis; hepatic stellate cells; pioglitazone
| The first 150 words of the full text of this article appear below. |
Liver tissue scarring, or fibrosis, is considered a common pathway leading to the alterations typical of cirrhosis, and delaying its progression likely results in longer patient survival and reduced need for liver transplantation. The past 15 years have witnessed a tremendous advance in our understanding of the cellular and molecular mechanisms responsible for the fibrogenic response in the liver (reviewed by Bataller and Brenner1). Damage to hepatocytes, or alterations in the biliary tree, activate mesenchymal cells that acquire a myofibroblastic phenotype, actively proliferate, produce extracellular matrix components, and secrete soluble mediators that contribute to maintenance of a chronic "wound healing" response, resulting in progressive scarring and alteration of the microvascular architecture. Activation of hepatic stellate cells (HSC) is considered a major source of myofibroblast-like cells during liver injury, together with the contribution of other myofibroblasts, such as those originating from the portal tracts.2 In spite of the
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Gut 2006 55: 1020-1029.[Abstract] [Full Text] [PDF]
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