线粒体功能障碍在肝纤维化发病中的作用机制
DOI: 10.12449/JCH260124
利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:洪雨蝶负责设计论文框架,撰写论文;郭锦晨负责拟定写作思路;施卫兵指导撰写文章并定稿;孙宇洁负责起草文章大纲;王佳敏负责整理机制图思路;高甜甜负责审阅文章。
Research advances in mitochondrial dysfunction in the pathogenesis of hepatic fibrosis
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摘要: 肝纤维化是在多种致病因素的影响下,肝内纤维结缔组织过度堆积并异常增生,可进展为肝硬化、门静脉高压及肝癌。其病理机制涉及肝细胞损伤、炎症细胞浸润与炎症介质释放、肝星状细胞活化以及细胞外基质堆积等。近年研究关注线粒体功能障碍在该疾病发展,包括代谢紊乱与能量不足、氧化应激、线粒体动态失衡、自噬功能改变等机制驱动肝纤维化的分子通路,这些均能引起肝损伤。本文综述了线粒体功能障碍在肝纤维化发病机制中的最新进展,可为临床治疗提供新治疗策略。Abstract: Hepatic fibrosis refers to excessive accumulation and abnormal proliferation of fibrous connective tissue in the liver triggered by multiple pathogenic factors, and it may progress to liver cirrhosis, portal hypertension, and liver cancer. The pathological mechanisms of hepatic fibrosis involve hepatocyte injury, inflammatory cell infiltration with the release of inflammatory mediators, hepatic stellate cell activation, and extracellular matrix deposition. Recent studies have focused on mitochondrial dysfunction in disease progression, including the molecular pathways for hepatic fibrosis driven by metabolic disorders, energy deficiency, oxidative stress, mitochondrial dynamic imbalance, and autophagic dysfunction, all of which can induce liver injury. This article reviews the latest advances in hepatic fibrosis, in order to provide new therapeutic strategies for clinical management.
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Key words:
- Hepatic Fibrosis /
- Mitochondria /
- Pathologic Processes
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