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Role of liver sinusoidal endothelial cell in metabolic dysfunction-associated fatty liver disease.
He, Qiongyao; He, Wu; Dong, Hui; Guo, Yujin; Yuan, Gang; Shi, Xiaoli; Wang, Dingkun; Lu, Fuer.
Affiliation
  • He Q; Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • He W; Division of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • Dong H; Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Wuhan, 430030, China.
  • Guo Y; Department of Integrated Traditional Chinese and Western Medicine, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • Yuan G; Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • Shi X; Department of Endocrinology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • Wang D; Department of Endocrinology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • Lu F; Department of Integrated Traditional Chinese and Western Medicine, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China. wdkung@163.com.
Cell Commun Signal ; 22(1): 346, 2024 Jun 28.
Article in En | MEDLINE | ID: mdl-38943171
ABSTRACT
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.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Endothelial Cells / Liver Limits: Animals / Humans Language: En Journal: Cell Commun Signal Year: 2024 Type: Article Affiliation country: China

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Endothelial Cells / Liver Limits: Animals / Humans Language: En Journal: Cell Commun Signal Year: 2024 Type: Article Affiliation country: China