The role of sex differences in autophagy in the heart during coxsackievirus B3-induced myocarditis

J Cardiovasc Transl Res. 2014 Mar;7(2):182-91. doi: 10.1007/s12265-013-9525-5. Epub 2013 Dec 10.

Abstract

Under normal conditions, autophagy maintains cardiomyocyte health and integrity through turnover of organelles. During stress, oxygen and nutrient deprivation, or microbial infection, autophagy prolongs cardiomyocyte survival. Sex differences in induction of cell death may to some extent explain the disparity between the sexes in many human diseases. However, sex differences in gene expression, which regulate cell death and autophagy, were so far not taken in consideration to explain the sex bias of viral myocarditis. Coxsackievirus B3 (CVB3)-induced myocarditis is a sex-biased disease, with females being substantially less susceptible than males and sex hormones largely determine this bias. CVB3 was shown to induce and subvert the autophagosome for its optimal viral RNA replication. Gene expression analysis on mouse and human, healthy and CVB3-infected, cardiac samples of both sexes, suggests sex differences in autophagy-related gene expression. This review discusses the aspects of sex bias in autophagy induction in cardiomyocytes.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Autophagy* / genetics
  • Coxsackievirus Infections / genetics
  • Coxsackievirus Infections / immunology
  • Coxsackievirus Infections / pathology*
  • Coxsackievirus Infections / virology*
  • Enterovirus B, Human / immunology
  • Enterovirus B, Human / pathogenicity*
  • Female
  • Gene Expression Regulation
  • Host-Pathogen Interactions
  • Humans
  • Male
  • Myocarditis / genetics
  • Myocarditis / immunology
  • Myocarditis / pathology*
  • Myocarditis / virology*
  • Myocytes, Cardiac / immunology
  • Myocytes, Cardiac / pathology*
  • Myocytes, Cardiac / virology*
  • Risk Assessment
  • Risk Factors
  • Sex Factors