Cross talk between mitochondria and NADPH oxidases.
Cross talk between mitochondria and NADPH oxidases.
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DOI：
10.1016/j.freeradbiomed.2011.06.033
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发表时间：
2011-10-01
影响因子：
7.4
通讯作者：
Dikalov, Sergey
中科院分区：
文献类型：
--
作者：
Dikalov, Sergey
关键词：
活性氧（Reactive oxygen species，ROS）在生理和病理过程中起着重要作用。近年来，已报道了ROS源的前馈调节。然而，ROS的主要细胞来源（如线粒体和NADPH氧化酶）之间的相互作用仍然不清楚。本文综述了线粒体和NADPH氧化酶之间的串扰在病理生理过程中的作用的最新发现。线粒体在细胞中具有最高水平的抗氧化剂，并在维持细胞氧化还原状态中发挥重要作用，从而充当ROS和氧化还原汇并限制NADPH氧化酶活性。然而，线粒体不仅是NADPH氧化酶产生的ROS的靶点，而且是ROS的重要来源，在某些条件下，ROS可以刺激NADPH氧化酶。因此，线粒体和NADPH氧化酶之间的这种串扰可能代表了ROS产生的前馈恶性循环，其可以在氧化应激条件下被靶向。已经证明，靶向抗氧化剂打破这种恶性循环，抑制线粒体产生ROS并降低NADPH氧化酶活性。这可能为治疗许多病理状况提供新的策略，包括衰老、动脉粥样硬化、糖尿病、高血压和退行性神经系统疾病，其中线粒体氧化应激似乎起作用。可以想象的是，使用靶向治疗将是有效的，在这些条件。
Reactive oxygen species (ROS) play an important role in physiological and pathological processes. In recent years, a feed-forward regulation of the ROS sources has been reported. The interaction between main cellular sources of ROS, such as mitochondria and NADPH oxidases, however, remain obscure. This work summarizes the latest findings on the role of crosstalk between mitochondria and NADPH oxidases in pathophysiological processes. Mitochondria have the highest levels of antioxidants in the cell and play an important role in the maintenance of cellular redox status, thereby acting as an ROS and redox sink and limiting NADPH oxidase activity. Mitochondria, however, are not only a target for ROS produced by NADPH oxidase but also a significant source of ROS, which under certain condition may stimulate NADPH oxidases. This crosstalk between mitochondria and NADPH oxidases, therefore, may represent a feed-forward vicious cycle of ROS production which can be pharmacologically targeted under conditions of oxidative stress. It has been demonstrated that mitochondria-targeted antioxidants break this vicious cycle, inhibiting ROS production by mitochondria and reducing NADPH oxidase activity. This may provide a novel strategy for treatment of many pathological conditions including aging, atherosclerosis, diabetes, hypertension and degenerative neurological disorders in which mitochondrial oxidative stress seems to play a role. It is conceivable that the use of mitochondria-targeted treatments would be effective in these conditions.
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