From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis

Abstract

Liver fibrosis is a key pathological process in the progression of chronic liver disease toward cirrhosis and liver failure. The development of liver fibrosis is closely related to a variety of etiologies, including alcoholic hepatitis, metabolic dysfunction-associated steatotic liver disease (MASLD), viral hepatitis, and drug-induced liver injury. Although advances in antiviral therapies for hepatitis B have contributed to a decline in its incidence, other etiologies such as MASLD and alcoholic hepatitis are becoming the main drivers for liver fibrosis. Currently, the management of liver fibrosis primarily focuses on controlling the underlying causes of liver fibrosis, including antiviral therapy and the cessation of alcohol or drug exposure. However, effective therapeutic options for advanced fibrosis remain limited, resulting in severe complications such as hepatic encephalopathy and portal hypertension, which markedly increase patient mortality and socio-economic burden. Therefore, early diagnosis and timely intervention for liver fibrosis are essential to prevent disease progression. With the ongoing advancement of modern molecular biology technologies, our understanding of the pathogenesis and pathophysiology of liver fibrosis continues to deepen. In this review, we summarize the molecular mechanisms, diagnostic approaches, current treatments, and potential therapeutic targets for liver fibrosis.

Keywords

Liver fibrosis / Hepatic stellate cells (HSCs) / Extracellular matrix (ECM) / Oxidative stress / Noninvasive diagnosis / Antifibrotic therapy

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