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线粒体功能障碍在高血压中的假定作用。

The putative role of mitochondrial dysfunction in hypertension.

作者信息

Puddu Paolo, Puddu Giovanni Maria, Cravero Eleonora, De Pascalis Susanna, Muscari Antonio

机构信息

Department of Internal Medicine, Cardioangiology, Hepatology, University of Bologna, Bologna, Italy.

出版信息

Clin Exp Hypertens. 2007 Oct;29(7):427-34. doi: 10.1080/10641960701613852.

Abstract

Hypertension is a condition associated with oxidative stress, endothelial dysfunction, and increased vascular resistance, representing probably both a cause and a consequence of elevated levels of reactive oxygen (ROS) and nitrogen (RNS) species. Mitochondria are important sites of ROS production, and a mitochondrial dysfunction, preceding endothelial dysfunction, might favor the development of hypertension. ROS production may also be induced by RNS, which inhibit the respiratory chain and may be generated through the action of a mitochondrial NO synthase. Mitochondrial uncoupling proteins are involved in both experimental and human hypertension. Finally, an excessive production of ROS may damage mitochondrial DNA, with resultant impairment in the synthesis of some components of the respiratory chain and further ROS production, a vicious cycle that may be implicated in hypertensive states.

摘要

高血压是一种与氧化应激、内皮功能障碍和血管阻力增加相关的病症,可能既是活性氧(ROS)和氮(RNS)水平升高的原因,也是其结果。线粒体是ROS产生的重要部位,在内皮功能障碍之前出现的线粒体功能障碍可能有利于高血压的发展。RNS也可能诱导ROS的产生,RNS抑制呼吸链,并且可能通过线粒体一氧化氮合酶的作用产生。线粒体解偶联蛋白与实验性高血压和人类高血压均有关。最后,ROS的过量产生可能会损伤线粒体DNA,导致呼吸链某些成分的合成受损以及进一步的ROS产生,这是一个可能与高血压状态有关的恶性循环。

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