首页|PPARγ在肝纤维化进程中的影响及其配体药物研发进展

PPARγ在肝纤维化进程中的影响及其配体药物研发进展

Effect of PPARγ in liver fibrosis and current development of its ligand drugs:research progress

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过氧化物酶体增殖激活受体(peroxisome proliferator-activated receptors,PPARs)是由内源性或外源性配体激活的核因子家族成员之一,是调节脂肪生成与代谢、炎症以及与其他转录因子信号等串扰在纤维化进程的调节剂,是近年来较有潜力的一个治疗靶点.肝纤维化(hepatic fibrosis,HF)是由多种病因导致的以胶原沉积、细胞外基质(extracellular matrix,ECM)增多为主的复杂病理变化,活化的肝星状细胞(hepatic stellate cells,HSCs)是其中心环节,随着对PPARs研究发现其亚型PPARγ在脂肪组织、巨噬细胞与HSCs的表达共同参与炎症反应等,进而导致肝纤维化的形成,其上调在逆转肝纤维化中维持HSCs静止表型及促使活化HSCs凋亡也起一定作用,表明以PPARγ为靶点激活的配体药物可能在抗纤维化治疗中扮演重要角色.
Peroxisome proliferator-activated receptors(PPARs)are members of the nuclear factor family activated by endogenous or exogenous ligands,which regulate adipogenesis and metabolism,inflammation and other transcriptional modulators of crosstalk such as factor signaling in fibrosis progression.They have become a promising therapeutic target in recent years.Hepatic fibrosis(HF)is a complex pathological change mainly caused by collagen deposition and extracellular matrix(ECM)increases due to various etiologies,in which activated hepatic stellate cells(HSCs)play a pivotal role.Studies on PPARs have found that the expressions of its isoform PPARγ in adipose tissue,macrophages and HSCs are involved in inflammation,which leads to the formation of liver fibrosis.The upregulation of PAARγ maintains HSCs in reversing liver fibrosis.The quiescent phenotype and the promotion of apoptosis of activated HSCs also make a difference,suggesting that ligand-activated drugs targeting PAARγ may play an important role in anti-fibrotic therapy.

PPARsPPARγliver fibrosishepatic stellate cellsligand drugdrug development

赵晓璐、高晓阳、张春艳、李明奇、马月宏

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内蒙古医科大学基础医学院,内蒙古 呼和浩特,010110

氧化物酶体增殖激活受体 PPARγ 肝纤维化 肝星状细胞 配体药物 药物研发

国家自然科学基金资助项目国家自然科学基金资助项目内蒙古自治区自然科学基金资助项目内蒙古自治区自然科学基金资助项目内蒙古自治区草原英才培养计划内蒙古医科大学致远人才项目内蒙古人才开发基金内蒙古医科大学重点项目内蒙古医科大学蒙药抗肝纤维化作用研究科技创新团队

81960759815607062019MS080102014MS0841ZY020101222056YKD2022ZD019YKD2022TD039

2024

10.19803/j.1672-8629.20230537

中国药物警戒
国家药品监督管理局药品评价中心（国家药品不良反应监测中心）

中国药物警戒

CSTPCD
影响因子：1.105
ISSN：1672-8629
年,卷(期)：2024.21(6)