纤维化
过氧化物酶体增殖物激活受体
脂肪性肝炎
脂肪变性
炎症
发病机制
肝纤维化
受体
核受体
癌症研究
脂质代谢
医学
氧化应激
生物
脂肪肝
内科学
内分泌学
转录因子
生物化学
疾病
基因
作者
Xin Han,Yan‐Ling Wu,Qiao Yang,Gang Cao
标识
DOI:10.1016/j.pharmthera.2020.107791
摘要
Liver fibrosis is a dynamic wound-healing process associated with the deposition of extracellular matrix produced by myofibroblasts. HSCs activation, inflammation, oxidative stress, steatosis and aging play critical roles in the progression of liver fibrosis, which is correlated with the regulation of the peroxisome proliferator-activated receptor (PPAR) pathway. As nuclear receptors, PPARs reduce inflammatory response, regulate lipid metabolism, and inhibit fibrogenesis in the liver associated with aging. Thus, PPAR ligands have been investigated as possible therapeutic agents. Mounting evidence indicated that some PPAR agonists could reverse steatohepatitis and liver fibrosis. Consequently, targeting PPARs might be a promising and novel therapeutic option against liver fibrosis. This review summarizes recent studies on the role of PPARs on the pathogenesis and treatment of liver fibrosis.
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