fibrosis

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Related to Fibrogenesis: fibrosis, fibrose

fibrosis

the formation of an abnormal amount of fibrous tissue in an organ or part as the result of inflammation, irritation, or healing
Collins Discovery Encyclopedia, 1st edition © HarperCollins Publishers 2005

fibrosis

[fī′brō·səs]
(medicine)
Growth of fibrous connective tissue in an organ or part in excess of that naturally present.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
Beuvon et al., "N-Acetylcysteine for the prevention of stricture after circumferential endoscopic submucosal dissection of the esophagus: a randomized trial in a porcine model," Fibrogenesis & Tissue Repair, vol.
To elucidate the underlying mechanisms of Proliverenol in the suppression of liver fibrogenesis, we measured the levels of TGF-[[beta].sub.1] in the rat model.
During this pathological process, hepatic stellate cells (HSCs) are the main executor of fibrogenesis. HSC activation increases the expression and secretion of collagen and other ECM components.
This proinflammatory environment is mainly due to the senescence-associated secretory phenotype (SASP) of the senescent immune cells [42,43], resembling on the one side the processes during chronic liver injury and fibrogenesis [45] and on the other side the processes in mitochondria and autophagy-inflammation-cell death axis, which are quite similar to those described for alcoholic hepatitis and NASH [46-49].
Future studies are required to determine the active ingredients and their amounts in hAMSC-CM, which may provide a new approach to treating liver fibrogenesis.
There are four main pathophysiological mechanisms involved in iron overload: increased absorption of dietary iron in the upper intestine, decreased expression of iron regulatory hormone hepcidin, altered function of HFE, and iron-elicited tissue injury with fibrogenesis [2].
The novel cardiac biomarker galectin-3 (Gal-3) is a beta galactoside binding lectin involved in fibrogenesis and inflammatory response in the failing heart.
Moreover, the activation of TLR9 in hepatic stellate cells suggests a role in promoting fibrogenesis [56].
Numerous studies suggest an association between an impaired immune response and clinical outcome, and there is evidence that immune cells modulate fibrogenesis of hepatitis C [3-5].
The injury process in ARDS involves a complex interaction of numerous factors, including inflammatory cytokines, epithelial and endothelial damage, fibrogenesis, and abnormal lung mechanics.
Hepatic fibrogenesis and transforming growth factor/Smad signaling activation in rats chronically exposed to low doses of lead.