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首页> 外文期刊>Progress in Cardiovascular Diseases >Mitochondrial DNA replication, nucleoside reverse-transcriptase inhibitors, and AIDS cardiomyopathy.
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Mitochondrial DNA replication, nucleoside reverse-transcriptase inhibitors, and AIDS cardiomyopathy.

机译：线粒体DNA复制，核苷逆转录酶抑制剂和AIDS心肌病。

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摘要

Nucleoside reverse-transcriptase inhibitors (NRTIs) in combination with other antiretrovirals (HAART) are the cornerstones of current AIDS therapy, but extensive use brought mitochondrial side effects to light. Clinical experience, pharmacological, cell, and molecular biological evidence links altered mitochondrial (mt-) DNA replication to the toxicity of NRTIs in many tissues, and conversely, mtDNA replication defects and mtDNA depletion in target tissues are observed. Organ-specific pathological changes or diverse systemic effects result from and are frequently attributed to HAART in which NRTIs are included. The shared features of mtDNA depletion and energy depletion became key observations and related the clinical and in vivo experimental findings to inhibition of mtDNA replication by NRTI triphosphates in vitro. Subsequent to those findings, other observations suggested that mitochondrial energy deprivation is concomitant with or the result of mitochondrial oxidative stress in AIDS (from HIV, for example) or from NRTI therapy itself.
机译：核苷类逆转录酶抑制剂（NRTIs）与其他抗逆转录病毒药物（HAART）的结合是当前AIDS治疗的基础，但广泛使用已使线粒体副作用显着。临床经验，药理学，细胞和分子生物学证据将线粒体（mt-）DNA复制的改变与NRTI在许多组织中的毒性联系在一起，相反，在目标组织中观察到mtDNA复制缺陷和mtDNA消耗。特定于器官的病理变化或各种全身效应是由HAART引起的，并经常归因于其中包含NRTI的HAART。 mtDNA消耗和能量消耗的共同特征成为关键观察，并将临床和体内实验结果与NRTI三磷酸盐体外抑制mtDNA复制有关。在这些发现之后，其他观察结果表明，线粒体能量剥夺与艾滋病（例如，来自艾滋病毒）或NRTI治疗本身的线粒体氧化应激同时发生或由其引起。

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