Sex differences in the myocardial inflammatory response to acute injury

Shock. 2005 Jan;23(1):1-10. doi: 10.1097/01.shk.0000148055.12387.15.


Hemorrhage, trauma, ischemia/reperfusion, burn, and sepsis each lead to cardiac dysfunction. These insults lead to an inflammatory cascade, which plays an important role in this process. Gender has been shown to influence the inflammatory response, as well as outcomes after acute injury. The mechanisms by which gender affects the inflammatory response to and the outcome of acute injury are being actively investigated. We searched PubMed for articles in the English language by using the search words sex, gender, estrogen, testosterone, inflammation, acute injury, ischemia reperfusion, sepsis, trauma, and burns. These were used in various combinations. We read the abstracts of the relevant titles to confirm their relevance, and the full articles were then extracted. References from extracted articles were checked for any additional relevant articles. This review will examine evidence for gender differences in the outcome to acute injury, explain the myocardial inflammatory response to acute injury, and elucidate the various mechanisms by which gender affects the myocardial response to acute injury.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Adenosine Triphosphate / chemistry
  • Adult
  • Antioxidants
  • Apoptosis
  • Burns / immunology
  • Cytokines / metabolism
  • Estrogens / metabolism
  • Female
  • Heart Injuries / immunology
  • Humans
  • Inflammation
  • Male
  • Middle Aged
  • Models, Biological
  • Myocardium / immunology*
  • Myocardium / pathology*
  • Nitric Oxide / metabolism
  • Potassium Channels / chemistry
  • PubMed
  • Reperfusion Injury
  • Sepsis / immunology
  • Sex Factors
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Antioxidants
  • Cytokines
  • Estrogens
  • Potassium Channels
  • Nitric Oxide
  • Adenosine Triphosphate
  • p38 Mitogen-Activated Protein Kinases