Review explores angiogenesis mechanisms in chronic inflammatory liver disease, suggesting anti-angiogenic therapy implications.
Angiogenesis is a key pathological process in chronic inflammatory liver diseases and contributes significantly to fibrosis progression and the development of portal hypertension. This review explores the cellular and molecular mechanisms that regulate angiogenesis in the chronically injured liver, highlighting the role of hepatic stellate cells, liver sinusoidal endothelial cells, inflammatory mediators, hypoxia‑induced pathways, and extracellular matrix remodeling. The article integrates experimental and clinical evidence to explain how persistent inflammation and hypoxia stimulate pro‑angiogenic signaling, ultimately promoting architectural distortion characteristic of advanced chronic liver disease. Understanding these mechanisms provides a biological basis for the potential use of anti‑angiogenic therapies in chronic liver disease and hepatocellular carcinoma.
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Chaparro et al. (2007) studied this question.
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