Role of liver sinusoidal endothelial cell in metabolic dysfunction-associated fatty liver disease

• Published in: Cell communication and signaling 2024-06, Vol.22 (1), p.346-18, Article 346
• Main Authors: He, Qiongyao, He, Wu, Dong, Hui, Guo, Yujin, Yuan, Gang, Shi, Xiaoli, Wang, Dingkun, Lu, Fuer
• Format: Article
• Language: English
• Subjects: Angiogenesis; Animals; Antigens; Blood cells; Blood pressure; Capillarization; Endothelial cells; Endothelial Cells - metabolism; Endothelial Cells - pathology; Endothelial dysfunction; Fatty liver; Fatty Liver - metabolism; Fatty Liver - pathology; Fibrosis; Hepatocytes; Humans; Immune system; Inflammation; Insulin resistance; Kinases; Lipids; Lipoproteins; Liver - metabolism; Liver - pathology; Liver cancer; Liver Cirrhosis - metabolism; Liver Cirrhosis - pathology; Liver diseases; Liver sinusoidal endothelial cells; Localization; Metabolism; Nitric oxide; Phenotypes; Proteins; Steatosis; Vascular endothelial growth factor
• ISSN: 1478-811X; 1478-811X
• DOI: 10.1186/s12964-024-01720-9

Liver sinusoidal endothelial cells (LSECs) are highly specialized endothelial cells that represent the interface between blood cells on one side and hepatocytes on the other side. LSECs not only form a barrier within the hepatic sinus, but also play important physiological functions such as regulating hepatic vascular pressure, anti-inflammatory and anti-fibrotic. Pathologically, pathogenic factors can induce LSECs capillarization, that is, loss of fenestra and dysfunction, which are conducive to early steatosis, lay the foundation for the progression of metabolic dysfunction-associated fatty liver disease (MAFLD), and accelerate metabolic dysfunction-associated steatohepatitis (MASH) and liver fibrosis. The unique localization, phenotype, and function of LSECs make them potential candidates for reducing liver injury, inflammation, and preventing or reversing fibrosis in the future.