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Throughout recent years, other enzymes and hormones have been identified as prompting antioxidant effects, although their mechanisms are not completely clear

On the other hand, a tyrosine kinase inhibitor, called nintedanib, primarily targets VEGF, FGF, and PDGF receptors and reduces ECM deposition and fibroblast proliferation [9, 14]

Excessive production of ECM components, coupled with chronic inflammation, promotes the progression from steatosis to hepatic fibrosis, cirrhosis, and ultimately liver failure (90)