Drug-Induced Mitochondrial Cardiomyopathy and Cardiovascular Risks in Children

Neha Bansal, Mariana Gerschenson, Tracie L. Miller, Stephen E. Sallan, Jason Czachor, Hiedy Razoky, Ashley Hill, Miriam Mestre, Steven E. Lipshultz

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations


This chapter describes the mechanisms and the short- and long-term consequences of human immunodeficiency virus (HIV) medications and cancer chemotherapies that are associated with mitochondrial dysfunction and its cardiac consequences in children. Adults and children with HIV are living longer because of advances in antiretroviral therapy (ART). Mitochondrial dysfunction secondary to ART is drug and organ specific. This specificity was first described in 1988, in HIV patients treated with high doses of the nucleoside reverse transcriptase inhibitor (NRTI), zidovudine. One of the major successes of pediatric oncology is that children with childhood cancers are living substantially longer and healthier lives because of advances in chemotherapeutic agents. Chemotherapeutic medications are designed to interfere with rapidly dividing neoplastic cells. However, in the process, they can adversely affect normal cell division, especially in tissues with rapid turnover.

Original languageEnglish (US)
Title of host publicationMitochondrial Dysfunction Caused by Drugs and Environmental Toxicants
Number of pages18
ISBN (Electronic)9781119329725
ISBN (Print)9781119329701
StatePublished - Feb 21 2018
Externally publishedYes


  • Antiretroviral therapy
  • Cardiac consequences
  • Chemotherapeutic medications
  • Human immunodeficiency virus
  • Mitochondrial cardiomyopathy
  • NRTI
  • Pediatric oncology

ASJC Scopus subject areas

  • Chemistry(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)


Dive into the research topics of 'Drug-Induced Mitochondrial Cardiomyopathy and Cardiovascular Risks in Children'. Together they form a unique fingerprint.

Cite this