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Life sciences · Journal article
Hepatoma Research · October 27, 2026
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Metabolic dysfunction-associated steatotic liver disease/ metabolic dysfunction-associated steatohepatitis (MASLD/MASH) has become a leading cause of advanced chronic liver disease and hepatocellular carcinoma (HCC). Among all histological features, liver fibrosis is the strongest predictor of liver-related outcomes and is increasingly recognized not only as a marker of disease severity but also as an active driver of hepatocarcinogenesis. Fibrosis promotes malignant transformation through persistent inflammation, extracellular matrix (ECM) remodeling, tissue stiffening, immune dysregulation, angiogenesis, genomic instability, and epigenetic reprogramming. Although lifestyle modification and metabolism-directed therapies can improve steatosis and steatohepatitis, established fibrosis often persists, underscoring the need for targeted antifibrotic strategies. This review summarizes the cellular and molecular mechanisms underlying MASLD-associated fibrogenesis, with particular emphasis on hepatic stellate cell activation, matrix turnover, inflammatory signaling, and fibrotic memory. We discuss current and emerging therapeutic approaches, including lifestyle-based interventions, incretin-based therapies, thyroid hormone receptor-β agonists, peroxisome proliferator-activated receptor (PPAR) agonists, fibroblast growth factor 21 (FGF21) analogs, immunomodulatory agents, and direct antifibrotic strategies targeting transforming growth factor beta (TGF-β), platelet-derived growth factor (PDGF), ECM remodeling, mechanotransduction, and myofibroblast persistence. Recent clinical trials demonstrate encouraging histological improvements, particularly with metabolism-directed and pleiotropic agents; however, no randomized trial has yet shown that fibrosis regression reduces HCC incidence. Reliable non-invasive biomarkers, molecular risk signatures, liquid biopsy approaches, and multi-omics-based precision medicine will therefore be essential to monitor fibrosis regression, identify residual cancer risk, and guide individualized surveillance. We propose that antifibrotic therapy in MASLD/MASH warrants consideration not only as a strategy for fibrosis reversal but also as a potential disease-modifying approach to interrupt fibrosis-driven hepatocarcinogenesis and reduce the long-term burden of HCC.