Pulmonary, Allergy and Critical Care Division, Emory University School of Medicine/Atlanta VA Medical Center, 1670 Clairmont Road, Mailstop 151P, Decatur, GA 30033, USA.
Free Radic Biol Med. 2012 Jul 1;53(1):143-59. doi: 10.1016/j.freeradbiomed.2012.03.019. Epub 2012 Apr 21.
Over 1 million people in the United States and 33 million individuals worldwide suffer from HIV/AIDS. Since its discovery, HIV/AIDS has been associated with an increased susceptibility to opportunistic infection due to immune dysfunction. Highly active antiretroviral therapies restore immune function and, as a result, people infected with HIV-1 are living longer. This improved survival of HIV-1 patients has revealed a previously unrecognized risk of developing vascular complications, such as atherosclerosis and pulmonary hypertension. The mechanisms underlying these HIV-associated vascular disorders are poorly understood. However, HIV-induced elevations in reactive oxygen species (ROS), including superoxide and hydrogen peroxide, may contribute to vascular disease development and progression by altering cell function and redox-sensitive signaling pathways. In this review, we summarize the clinical and experimental evidence demonstrating HIV- and HIV antiretroviral therapy-induced alterations in reactive oxygen species and how these effects are likely to contribute to vascular dysfunction and disease.
超过 100 万美国人以及全球 3300 万人患有 HIV/AIDS。自发现以来，由于免疫功能障碍，HIV/AIDS 与机会性感染的易感性增加有关。高效抗逆转录病毒疗法恢复了免疫功能，因此，感染 HIV-1 的人寿命更长。HIV-1 患者的这种存活率提高揭示了以前未被认识到的血管并发症风险，例如动脉粥样硬化和肺动脉高压。这些与 HIV 相关的血管疾病的发病机制尚不清楚。然而，HIV 诱导的活性氧（ROS）升高，包括超氧阴离子和过氧化氢，可能通过改变细胞功能和氧化还原敏感信号通路来促进血管疾病的发生和发展。在这篇综述中，我们总结了临床和实验证据，证明 HIV 和 HIV 抗逆转录病毒治疗会引起活性氧的改变，以及这些影响如何可能导致血管功能障碍和疾病。
