Review of Liver Fibrosis and Inflammation

¹ Beijing Forestry University, School of Biological Sciences and Technology, No. 35 Qinghua East Road, Haidian District, Beijing, 100083, China
² The University of British Columbia, Faculty of Forestry, 2424 Main Mall Vancouver, BC Canada V6T 1Z4

^* Corresponding author: This email address is being protected from spambots. You need JavaScript enabled to view it.

Abstract

Liver fibrosis is a common pathological process triggered by chronic liver diseases (such as viral hepatitis, non-alcoholic fatty liver disease, and alcoholic liver disease), posing a serious threat to global public health. This article provides a systematic review of the epidemiology, pathogenesis, major cell types, key signaling pathways, and treatment advances in liver fibrosis. The core of fibrosis lies in the activation of hepatic stellate cells (HSCs) and their sustained synthesis of extracellular matrix (ECM). Macrophages, as important immune regulatory cells, play a bidirectional regulatory role in inflammatory responses and fibrosis reversal. The paper focuses on elucidating the regulatory mechanisms of immune activation mediated by DAMPs/PAMPs, TGF- ß /Smad, and PDGF signaling pathways on HSC activation, as well as the polarization dynamics of M1/M2 macrophages. Research has shown that liver fibrosis has a certain degree of reversibility, and early intervention can promote the inactivation or apoptosis of activated HSCs, restoring tissue structure. Based on these mechanisms, drugs targeting key factors such as CCL2/CCR2 and TGF- ß , as well as emerging therapeutic approaches like stem cells, gene editing, and gut microbiota modulation, have become key directions for future treatment. Although no specific anti-fibrotic drugs have been approved yet, mechanistic research provides a solid foundation for personalized precision therapy.