
FOLLOWUS
1. Department of Gastroenterology, Affiliated Nanhua Hospital of University of South China,Hunan,Hengyang,China,421000
2. ,China
3. Department of Hematology
4. Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University,Shanghai,China,200025
网络出版日期:2013-12-31,
纸质出版日期:2013
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Xin-yan Jing, Xue-feng Yang, Kai Qing, 等. Roles of the Lipid Metabolism in Hepatic Stellate Cells Activation△[J]. 中国医学科学杂志(英文版), 2013,28(4):233-236.
Xin-yan Jing, Xue-feng Yang, Kai Qing, et al. Roles of the Lipid Metabolism in Hepatic Stellate Cells Activation[J]. Chinese medical sciences journal, 2013, 28(4): 233-236.
Xin-yan Jing, Xue-feng Yang, Kai Qing, 等. Roles of the Lipid Metabolism in Hepatic Stellate Cells Activation△[J]. 中国医学科学杂志(英文版), 2013,28(4):233-236. DOI:
Xin-yan Jing, Xue-feng Yang, Kai Qing, et al. Roles of the Lipid Metabolism in Hepatic Stellate Cells Activation[J]. Chinese medical sciences journal, 2013, 28(4): 233-236. DOI:
The lipids present in hepatic stellate cells (HSCs) lipid droplets include retinyl ester
triglyceride
cholesteryl ester
cholesterol
phospholipids and free fatty acids. Activation of HSCs is crucial to the development of fibrosis in liver disease. During activation
HSCs transform into myofibroblasts with concomitant loss of their lipid droplets and production of excessive extracellular matrix. Release of lipid droplets containing retinyl esters and triglyceride is a defining feature of activated HSCs. Accumulating evidence supports the proposal that recovering the accumulation of lipids would inhibit the activation of HSCs. In healthy liver
quiescent HSCs store 80% of total liver retinols and release them depending on the extracellular retinol status. However
in injured liver activated HSCs lose their retinols and produce a considerable amount of extracellular matrix
subsequently leading to liver fibrosis. Further findings prove that lipid metabolism of HSCs is closely associated with its activation
yet relationship between activated HSCs and the lipid metabolism has remained mysterious.
The lipids present in hepatic stellate cells (HSCs) lipid droplets include retinyl ester
triglyceride
cholesteryl ester
cholesterol
phospholipids and free fatty acids. Activation of HSCs is crucial to the development of fibrosis in liver disease. During activation
HSCs transform into myofibroblasts with concomitant loss of their lipid droplets and production of excessive extracellular matrix. Release of lipid droplets containing retinyl esters and triglyceride is a defining feature of activated HSCs. Accumulating evidence supports the proposal that recovering the accumulation of lipids would inhibit the activation of HSCs. In healthy liver
quiescent HSCs store 80% of total liver retinols and release them depending on the extracellular retinol status. However
in injured liver activated HSCs lose their retinols and produce a considerable amount of extracellular matrix
subsequently leading to liver fibrosis. Further findings prove that lipid metabolism of HSCs is closely associated with its activation
yet relationship between activated HSCs and the lipid metabolism has remained mysterious.
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