Hepatic stellate cells role in the course of metabolic disorders development – A molecular overview

肝星状细胞 脂毒性 转分化 细胞生物学 趋化因子 细胞外基质 肌成纤维细胞 脂肪肝 医学 肝纤维化 纤维化 炎症 肝细胞学 干细胞 生物 胰岛素抵抗 免疫学 胰岛素 内分泌学 病理 疾病 肝脏代谢
作者
Nabila Bourebaba,Krzysztof Marycz
出处
期刊:Pharmacological Research [Elsevier BV]
卷期号:170: 105739-105739 被引量:38
标识
DOI:10.1016/j.phrs.2021.105739
摘要

Fibrosis is characterized by an abnormal accumulation of extracellular matrix (ECM) constituents in the liver parenchyma that lead to hepatic cirrhosis. After liver injury, the hepatic stellate cells (HSCs) undergo a response called "activation", transforming the cells into proliferative, fibrogenic and contractile myofibroblasts, representing the main collagen-producing cells in the injured tissue. Activated HSCs are considered as pro-inflammatory cells producing cytokines and several hepatomatogens; they are additionally involved in the recruitment of Kupffer cells, circulating monocytes and macrophages through the production of chemokines. Moreover, HSC have been proposed as being involved in the development of insulin resistance mainly mediated by their inflammatory properties, which undeniably links their activation to the development of diabetes and Non-alcoholic fatty liver disease. In addition, when the liver is injured, a complex interaction between hepatocytes and HSCs occurs, inducing mitochondrial dysfunction, which contributes to the accumulation of fats in hepatocytes that trigger to liver lipotoxicity. These mechanisms underlying the activation of HSC suggest their major role in the development of metabolic disorders. It turns out that several molecules including MicroRNAs and proteins have the ability to inhibit the activation and the proliferation of HSCs, which makes them interesting therapeutic targets for the subsequent management of metabolic conditions. This review focuses on the mechanisms and molecular pathways underlying the initiation and onset of metabolic disorders following HSCs activation, as well as on molecular therapeutic targets, which could limit their fibrogenic transdifferentiation and therefore improve the liver condition in the course of metabolic imbalance.
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