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药物诱导肝硬化症中的线粒体功能障碍:最近的发现和当前的概念

Annie Borgne-Sanchez¹, Bernard Fromenty²

¹MITOLOGICS S.A.S., 172 rue de Charonne, 75011 Paris, France.

Clinics and research in hepatology and gastroenterology

|January 11, 2025

概括

药物诱导的线粒体功能障碍会损害脂肪酸氧化 (FAO),导致肝脏肥胖症. 监测患有代谢功能障碍相关的脂肪性肝病 (MASLD) 的患者,并考虑像l-carnitine这样的疗法,可以预防肝损伤.

科学领域:

肝病学肝病学是一种肝病学.
线粒体生物学线粒体生物学
药物毒理学药物毒理学

背景情况:

线粒体脂肪酸氧化 (FAO) 对于肝脏能量生产和脂质平衡至关重要,由线粒体呼吸链 (MRC) 和PPARα.
药物诱导的线粒体功能障碍可能会导致肝损伤,从微带状脂肪炎到脂肪肝炎和肝硬化,这取决于FAO损伤的严重程度.
机制包括直接的酶抑制,协酶A/l-卡尼分离,MRC复合物功能障碍和降低PPARα表达,氧化应激在疾病进展中起着关键作用.

研究的目的:

审查药物诱导线粒体功能障碍和随后的肝损伤的机制.
讨论药物诱导的肥胖症和肥胖肝炎的临床影响,特别是在MASLD患者中.
探索潜在的治疗策略,以缓解药物诱导的线粒体功能障碍和肝脏疾病.

主要方法:

对药物诱导的肝损伤的文献综述,重点关注线粒体通路.
分析影响脂肪酸氧化和脂质代谢的机制.
综合有关临床结果和治疗干预措施的信息.

主要成果:

药物诱导的线粒体功能障碍会损害FAO,导致不同程度的肥胖症 (微型或宏型).
进展为脂肪肝炎和肝硬化与线粒体功能障碍,氧化应激和潜在的非线粒体因素,如改变的脂质生成有关.
患有MASLD的患者有更高的药物诱导肝损伤风险,需要仔细监测.

结论:

线粒体功能障碍是药物诱导的肝硬化和肝硬化性肝炎的中心机制.
建议密切监测和潜在的治疗干预措施 (例如,l-carnitine,N-乙半氨酸) 适用于使用线粒体毒药物治疗的MASLD患者.
了解这些途径对于预防和管理药物诱导的肝病至关重要.

关键词:

药物药物药物药物药物肝脏肝脏肝脏肝脏线粒体中的线粒体.这种疾病叫做steatosis.有毒性有毒性

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