Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells

• Published in: Molecular biology reports 2021-02, Vol.48 (2), p.1915-1924
• Main Authors: Shu, Yongxiang, Liu, Xuyou, Huang, Haifeng, Wen, Qi, Shu, Jianchang
• Format: Article
• Language: English
• Subjects: Animal Anatomy; Animal Biochemistry; Antioxidants; Apoptosis; Autophagy; Biodegradation; Biomedical and Life Sciences; Collagen; Extracellular matrix; Fibrosis; Hepatocytes; Histology; Inflammation; Kupffer cells; Life Sciences; Liver; Liver diseases; Mini Review; Mini Review Article; Morphology; Organelles; Oxidative stress; Pathogenesis; Phagocytosis; Reactive oxygen species; Stellate cells; Wound healing
• ISSN: 0301-4851; 1573-4978
• DOI: 10.1007/s11033-021-06171-w

Chronic liver diseases caused by various pathogenesis are marked by inflammatory infiltration and wound healing reaction, while their normal regeneration ability is impaired. The unbalance between the generation and the degradation of extracellular matrix (ECM) leads to collagen accumulation and develops into liver fibrosis. Inflammation, oxidative stress, and autophagy interact closely in the pathogenesis of hepatic fibrosis. Reactive Oxygen Species (ROS) can not only stimulate Kupffer cells to release massive inflammatory factors, but induce autophagy. However, the latter may suppress inflammatory reaction by inhibiting proinflammatory complex formation directly, and removing damaged organelles or pathogenic microorganism indirectly. At present, effective anti-fibrosis drugs are still lacking. Previous studies have found various natural compounds enabled liver protection through anti-inflammatory, antioxidant, and other mechanisms. In recent years, autophagy, a vital life activity, has been found to be involved in the mechanism of liver fibrosis. As a new target, developing anti-liver fibrosis drugs that regulate the activity of autophagy is very promising. In this review, we summarize the latest studies about natural compounds in the treatment of liver fibrosis by regulating autophagy.