Liver fibrosis

Liver fibrosis is a pathological process characterized by the excessive accumulation of extracellular matrix proteins, particularly collagen, which occurs in response to chronic liver injury from factors such as alcohol, viral infection, or metabolic dysfunction. It is not a single molecular target or receptor but rather a complex disease state and wound-healing response mediated by the activation of hepatic stellate cells and inflammatory signaling. While it is a major focus for drug development, pharmaceutical interventions actually target specific proteins within the fibrotic cascade, such as TGF-beta receptors, farnesoid X receptors (FXR), or thyroid hormone receptors. Over time, persistent fibrosis can progress to cirrhosis, leading to impaired organ function, portal hypertension, and increased risk for hepatocellular carcinoma (StatPearls, 2023; PubMed, 2022). Efforts to treat liver fibrosis currently focus on both treating the underlying cause of injury and directly modulating the cellular pathways responsible for scarring.

Other names

Hepatic fibrosisLiver scarringAdvanced liver scarringCirrhosis (end-stage)

Therapeutic strategies aimed at treating liver fibrosis generally target specific molecular pathways to inhibit the activation of hepatic stellate cells, reduce the expression of pro-fibrogenic cytokines like TGF-beta, or promote the degradation of excess extracellular matrix proteins (StatPearls, 2023; NIH, 2023).