Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The understanding of the cellular and molecular mechanisms of the fibrotic wound-healing response of the liver has made dramatic progress in the past 20 years. Hepatic stellate cells (HSCs), which after liver injury proliferate and transdifferentiate to myofibroblasts, have emerged as the primary source of the fibrotic response, even though other fibrogenic cells may also contribute to the production of extracellular matrix (ECM). Advances in the understanding of HSC regulation include apoptotic signaling, angiogenic signaling, and responses to oxidative stress. The ECM has emerged not only as a structural scaffold, but also as a dynamic and interactive matrix regulating stellate cell activation. Additionally, the innate immune system and immune signaling, as well as a broadening understanding of the transcriptional regulation including microRNAs and epigenetic events offer potential therapeutic targets. Unraveling genetic determinants related to mechanisms of hepatic fibrogenesis promise individualized therapy or prevention. Hepatic fibrosis and cirrhosis have emerged as treatable and potentially reversible consequence of chronic liver disease.
Prog Mol Biol Transl Sci 2010
PMID:Fibrosis in the liver: acute protection and chronic disease. 2107 33

Hepatic fibrosis and cirrhosis are chronic diseases affecting liver and a major health problem throughout the world. The hallmark of fibrosis and cirrhosis is inordinate synthesis and deposition of fibril forming collagens in the extracellular matrix of the liver leading to nodule formation and loss of normal architecture. Hepatic stellate cells play a crucial role in the pathogenesis and progression of liver fibrosis through secretion of several potent fibrogenic factors that trigger hepatocytes, portal fibrocytes, and bone marrow-derived fibroblasts to synthesize and deposit several connective tissue proteins, especially collagens between hepatocytes and space of Disse. Regulation of various events involved in the activation and transformation of hepatic stellate cells seems to be an appropriate strategy for the arrest of hepatic fibrosis and liver cirrhosis. In order to unravel the molecular mechanisms involved in the pathogenesis and progression of hepatic fibrosis, to determine proper and potent targets to arrest fibrosis, and to discover powerful therapeutic agents, a quick and reproducible animal model of hepatic fibrosis and liver cirrhosis that display all decompensating features of human condition is required. This review thoroughly evaluates the biochemical, histological, and pathological features of N-nitrosodimethylamine-induced model of liver injury, hepatic fibrosis, and early cirrhosis in rodents.
J Mol Med (Berl) 2020 Sep
PMID:Metabolism of N-nitrosodimethylamine, methylation of macromolecules, and development of hepatic fibrosis in rodent models. 3266 46