Journal
TRENDS IN PHARMACOLOGICAL SCIENCES
Volume 32, Issue 12, Pages 715-725Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2011.07.007
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Funding
- CIBER [CD06/04/0071]
- VALi + D contract [APOSTD/2011/049]
- [PI081325]
- [ACOMP/2010/207]
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The combined pharmacological approach to the treatment of HIV infection, known as highly active antiretroviral therapy (HAART), has dramatically reduced AIDS-related morbidity and mortality. However, its use has been associated with serious adverse reactions, of which those resulting from mitochondrial dysfunction are particularly widespread. Nucleos(t)ide-reverse transcriptase inhibitors (NRTIs) have long been considered the main source of HAART-related mitochondrial toxicity due to their ability to inhibit Poky, the DNA polymerase responsible for the synthesis of mitochondria! DNA. Nevertheless, accumulating evidence points to a more complex relationship between these organelles and NRTIs. Also, alternative pathways by which other groups of anti-HIV drugs (non-nucleoside reverse transcriptase inhibitors and protease inhibitors) interfere with mitochondria have been suggested, although their implications, both pharmacological and clinical, are open to debate. This review aims to provide a comprehensive overview of the mechanisms and factors which influence the mitochondrial involvement in the toxicity of all three major classes of anti-HIV drugs.
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