ROS/RNS as molecular signatures of chronic liver diseases

被引:45
作者
Che, Zhaodi [1 ]
Zhou, Ziyuan [2 ]
Li, Si-Qi [3 ]
Gao, Lei [4 ]
Xiao, Jia [5 ]
Wong, Nai-Kei [3 ]
机构
[1] Jinan Univ, Clin Res Inst, Inst Obes & Metab, Affiliated Hosp 1, Guangzhou 510000, Peoples R China
[2] Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp & Shenzhen Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc, Shenzhen 518116, Peoples R China
[3] Shantou Univ, Dept Pharmacol, Clin Pharmacol Sect, Med Coll, Shantou 515041, Peoples R China
[4] Southern Med Univ, Sch Tradit Chinese Med, Guangzhou 510000, Peoples R China
[5] Univ Hlth & Rehabil Sci, Qingdao Hosp, Shandong Prov Key Lab Clin Res Liver Dis, Qingdao 266001, Peoples R China
基金
中国国家自然科学基金;
关键词
RECEPTOR AGONIST TIRZEPATIDE; CELL-DEATH; NONALCOHOLIC STEATOHEPATITIS; SIGNALING PATHWAY; DUAL GIP; FIBROSIS; FERROPTOSIS; INJURY; ACTIVATION; METABOLISM;
D O I
10.1016/j.molmed.2023.08.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The liver can succumb to oxidant damage during the development of chronic liver diseases. Despite their physiological relevance to hepatic homeostasis, excessive reactive oxygen/nitrogen species (ROS/RNS) production under pathological con-ditions is detrimental to all liver constituents. Chronic oxidative stress coupled to unresolved inflammation sets in motion the activation of profibrogenic hepatic stellate cells (HSCs) and later pathogenesis of liver fibrosis, cirrhosis, and liver cancer. The liver antioxidant and repair systems, along with autophagic and ferroptotic machineries, are implicated in the onset and trajectory of disease development. In this review, we discuss the ROS/RNS-related mechanisms underlying liver fibrosis of distinct etiologies and highlight preclinical and clinical trials of antifibrotic therapies premised on remediating oxidative/nitrosative stress in hepatocytes or targeting HSC activation.
引用
收藏
页码:951 / 967
页数:17
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