R. Christopher Benyon

TL;DR: Following liver injury, hepatic stellate cells become activated and express a combination of matrix metalloproteinases (MMPs) and their specific tissue inhibitors (TIMPs) and TIMP-1 in particular is rapidly downregulated.

TL;DR: Recovery from comparatively advanced cirrhosis is possible and results in remodeling from a micronodular Cirrhosis to a macronsodular cir rhosis, which is suggested to be limited by tTg-mediated matrix cross-linking and a failure of HSC apoptosis.

TL;DR: An association between MMP13 expression and the presence of SAMs in the regression of experimental liver fibrosis is demonstrated and SAMs selectively, during resolution of fibrosis induce and use the major collagenase M MP13 to mediate the resorption of interstitial matrix and successfully remodel the fibrotic liver.

TL;DR: A mechanism by which the desmoplastic reaction in pancreatic cancer may form and, via the collagen within it, promote the malignant phenotype of Pancic cancer cells is elucidated, suggesting significant detriment to the host.

TL;DR: The studies suggest that αvβ3 integrin regulates the fate of hepatic stellate cells, and degradation of αv β3 ligands surrounding activated stellates cells during resolution of liver fibrosis might decrease α vβ3 integration ligation, suppressingStellate cell proliferation and inducing a fibrolytic, matrix metalloproteinase-secreting phenotype that may prime stellated cells for apoptosis.