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논문 기본 정보

자료유형
학술저널
저자정보
Jiaorong Qu (School of Life Sciences, Beijing University of Chinese Medicine;) Le Wang (School of Life Sciences, Beijing University of Chinese Medicine) Yufei Li (School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China) Xiaojiaoyang Li (School of Life Sciences, Beijing University of Chinese Medicine)
저널정보
대한간학회 Clinical and Molecular Hepatology Clinical and Molecular Hepatology Vol.30 No.3
발행연도
2024.7
수록면
303 - 325 (23page)

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초록· 키워드

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Liver sinusoidal endothelial cells (LSECs) are liver-specific endothelial cells with the highest permeability than other mammalian endothelial cells, characterized by the presence of fenestrae on their surface, the absence of diaphragms and the lack of basement membrane. Located at the interface between blood and other liver cell types, LSECs mediate the exchange of substances between the blood and the Disse space, playing a crucial role in maintaining substance circulation and homeostasis of multicellular communication. As the initial responders to chronic liver injury, the abnormal LSEC activation not only changes their own physicochemical properties but also interrupts their communication with hepatic stellate cells and hepatocytes, which collectively aggravates the process of liver fibrosis. In this review, we have comprehensively updated the various pathways by which LSECs were involved in the initiation and aggravation of liver fibrosis, including but not limited to cellular phenotypic change, the induction of capillarization, decreased permeability and regulation of intercellular communications. Additionally, the intervention effects and latest regulatory mechanisms of anti-fibrotic drugs involved in each aspect have been summarized and discussed systematically. As we studied deeper into unraveling the intricate role of LSECs in the pathophysiology of liver fibrosis, we unveil a promising horizon that pave the way for enhanced patient outcomes.

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