Mitochondria and sex-specific cardiac function

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The focus of this chapter is the gender differences in mitochondria in cardiovascular disease. There is broad evidence suggesting that some of the gender differences in cardiovascular outcome may be partially related to differences in mitochondrial biology (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017)). Mitochondrial disorders are causally affected by mutations in either nuclear or mitochondrial genes involved in the synthesis of respiratory chain subunits or in their posttranslational control. This can be due to mutations of the mtDNA which are transmitted by the mother or mutations in the nuclear DNA. Because natural selection on mitochondria operates only in females, mutations may have had more deleterious effects in males than in females (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017; Camara AK, Lesnefsky EJ, Stowe DF. Antioxid Redox Signal 13(3):279–347, 2010). As mitochondrial mutations can affect all tissues, they are responsible for a large panel of pathologies including neuromuscular disorders, encephalopathies, metabolic disorders, cardiomyopathies, neuropathies, renal dysfunction, etc. Many of these pathologies present sex/gender specificity. Thus, alleviating or preventing mitochondrial dysfunction will contribute to mitigating the severity or progression of the development of diseases. Here, we present evidence for the involvement of mitochondria in the sex specificity of cardiovascular disorders.

Original languageEnglish
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer New York LLC
Pages241-256
Number of pages16
DOIs
Publication statusPublished - Jan 1 2018

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1065
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Keywords

  • Aging heart
  • Apoptotic bodies
  • Autophagy
  • Calcium overload
  • Dynamin
  • Heart failure
  • Ischemic preconditioning
  • Krebs cycle
  • Mitochondrial biology
  • Mitochondrial dysfunction
  • Mitophagy
  • Mutations of mtDNA
  • Nuclear respiratory factor
  • Reactive oxygen species
  • Redox messenger

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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