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Roles of TGF-beta in hepatic fibrosis.

The ubiquitous pathophysiologic relevance of TGF-beta suggests its measurement in blood as a diagnostic tool and the importance of cross-talk among different signaling pathways to either specify, enhance, or inhibit T GF-beta responses.
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Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-β as major players and therapeutic targets

The present review summarises the actual knowledge on the pathogenesis of hepatic fibrogenesis, the role of transforming growth factor‐β and its signalling pathways in promoting the fibrogenic response, and the therapeutic modalities that are presently in the spotlight of many investigations and are already on the way to take the plunge into clinical studies.
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Hepatic recruitment of the inflammatory Gr1+ monocyte subset upon liver injury promotes hepatic fibrosis

Subpopulations of infiltrating monocytes in acute and chronic carbon tetrachloride‐induced liver injury in mice are characterized and inflammatory Gr1+ monocytes, recruited into the injured liver via CCR2‐dependent bone marrow egress, promote the progression of liver fibrosis.
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Cellular and molecular functions of hepatic stellate cells in inflammatory responses and liver immunology.

The role of HSC as central regulators of liver immunology may lead to novel therapeutic strategies for chronic liver diseases, and current directions of research investigate the immune-modulating functions of H SC in the environment of liver tumors, cellular heterogeneity or interactions promoting HSC deactivation during resolution of liver fibrosis.
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Biomarkers of liver fibrosis: clinical translation of molecular pathogenesis or based on liver-dependent malfunction tests.

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Antagonism of the chemokine Ccl5 ameliorates experimental liver fibrosis in mice.

The results define a successful therapeutic approach to reduce experimental liver fibrosis by antagonizing Ccl5 receptors and show that treatment with the CCL5 receptor antagonist Met-CCL5 inhibited cultured stellate cell migration, proliferation, and chemokine and collagen secretion.
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Ito cells are liver-resident antigen-presenting cells for activating T cell responses.

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Functional Contribution of Elevated Circulating and Hepatic Non-Classical CD14+CD16+ Monocytes to Inflammation and Human Liver Fibrosis

The expansion of CD14+CD16+ monocytes in the circulation and liver of CLD-patients upon disease progression is demonstrated and their functional contribution to the perpetuation of intrahepatic inflammation and profibrogenic HSC activation in liver cirrhosis is suggested.
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Diethylnitrosamine (DEN)-induced carcinogenic liver injury in mice

The outcome of liver injury after the application of DEN in mice appears to be a suitable animal model for the analysis of some aspects and processes that promote the pathogenesis of hepatocellular carcinoma in humans.
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The PDGF system and its antagonists in liver fibrosis.

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