Abstract
Acquired immune deficiency syndrome (AIDS) is a global epidemic that continues to escalate. Recent World Health Organization (WHO) estimates include over 33 million people currently diagnosed with human immunodeficiency virus (HIV)/AIDS. Twenty million HIV-infected individuals died over the past quarter century. Antiretrovirals, particularly nucleoside reverse transcriptase inhibitors (NRTIs), changed HIV/AIDS from a fatal disease to a chronic illness. Cardiomyopathy (CM) is a bona fide HIV/AIDS comorbidity. It may result from individual or combined effects of the HIV per se, immune reactions to it, or from toxicities of NRTIs. Clinical observations, in vitro and in vivo evidence, suggest various mechanisms of CM are centered around NRTI toxicity to mitochondria. This review highlights some of the hypotheses and data that support those hypotheses that focus on cardiotoxicity of NRTIs and on mitochondrial-associated pathways of NRTI toxicity in CM.
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