线粒体脂质氧化的病理生理学：4-羟基壬烯醛（4-HNE）和其他生物活性脂质在线粒体中的作用。,Free Radical Biology and Medicine

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线粒体脂质氧化的病理生理学：4-羟基壬烯醛（4-HNE）和其他生物活性脂质在线粒体中的作用。
Free Radical Biology and Medicine ( IF 7.1 ) Pub Date : 2017-05-01 , DOI: 10.1016/j.freeradbiomed.2017.04.363
Mengqing Xiao ₁ , Huiqin Zhong ₂ , Lin Xia ₃ , Yongzhen Tao ₃ , Huiyong Yin ₄

Affiliation

线粒体脂质对于维持线粒体膜的完整性和线粒体的正常功能至关重要。线粒体作为细胞的“动力源”，也是细胞中活性氧（ROS）的主要来源。当抗氧化剂系统被过量生产的ROS淹没时，就会发生氧化应激。线粒体膜中的多不饱和脂肪酸是ROS攻击的主要靶标，可能导致脂质过氧化（LPO）和反应性脂质（如4-羟基壬烯醛）的产生。当线粒体脂质被氧化时，线粒体的完整性和功能可能受到损害，最终可能导致线粒体功能障碍，这与许多人类疾病有关，包括癌症，心血管疾病，糖尿病和神经退行性疾病。线粒体脂质如何被氧化以及与线粒体LPO相关的潜在分子机制和病理生理后果仍然不清楚。线粒体特异性磷脂心磷脂的氧化和通过线粒体LPO生成生物活性脂质已被越来越多地认为是协调细胞凋亡，能量产生的代谢重编程，线粒体和免疫反应的重要事件。在这篇综述中，我们重点关注线粒体LPO和线粒体中生物活性脂质介体的产生如何在与氧化应激相关的人类相关疾病的背景下参与线粒体功能的调节。

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Pathophysiology of mitochondrial lipid oxidation: Role of 4-hydroxynonenal (4-HNE) and other bioactive lipids in mitochondria.

Mitochondrial lipids are essential for maintaining the integrity of mitochondrial membranes and the proper functions of mitochondria. As the "powerhouse" of a cell, mitochondria are also the major cellular source of reactive oxygen species (ROS). Oxidative stress occurs when the antioxidant system is overwhelmed by overproduction of ROS. Polyunsaturated fatty acids in mitochondrial membranes are primary targets for ROS attack, which may lead to lipid peroxidation (LPO) and generation of reactive lipids, such as 4-hydroxynonenal. When mitochondrial lipids are oxidized, the integrity and function of mitochondria may be compromised and this may eventually lead to mitochondrial dysfunction, which has been associated with many human diseases including cancer, cardiovascular diseases, diabetes, and neurodegenerative diseases. How mitochondrial lipids are oxidized and the underlying molecular mechanisms and pathophysiological consequences associated with mitochondrial LPO remain poorly defined. Oxidation of the mitochondria-specific phospholipid cardiolipin and generation of bioactive lipids through mitochondrial LPO has been increasingly recognized as an important event orchestrating apoptosis, metabolic reprogramming of energy production, mitophagy, and immune responses. In this review, we focus on the current understanding of how mitochondrial LPO and generation of bioactive lipid mediators in mitochondria are involved in the modulation of mitochondrial functions in the context of relevant human diseases associated with oxidative stress.

更新日期：2019-11-01

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