Heat shock protein 27: clue to understanding estrogen-mediated atheroprotection?

Trends Cardiovasc Med. 2010 Feb;20(2):54-8. doi: 10.1016/j.tcm.2010.03.008.

Abstract

Although the use of estrogen replacement therapy for postmenopausal women has been dramatically curtailed due to an unfavorable risk-benefit profile, there remains strong experimental evidence that ovarian hormones have a favorable effect on vessel wall homeostasis. We recently discovered that release of heat shock protein 27 (HSP27) into the serum is atheroprotective and mediated by ovarian hormones, preferentially functioning via estrogen receptor-beta. HSP27 binds scavenger receptor-A, reduces cholesterol uptake in macrophages, and attenuates mediators of vascular inflammation. Therefore, it is attractive to consider HSP27 as the active foot soldier of estrogens and potentially a novel therapeutic opportunity for vascular disease.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / metabolism*
  • Atherosclerosis / prevention & control*
  • Disease Models, Animal
  • Estrogen Receptor alpha / metabolism
  • Estrogen Receptor beta / metabolism
  • Estrogens / metabolism*
  • Female
  • HSP27 Heat-Shock Proteins / blood
  • HSP27 Heat-Shock Proteins / metabolism*
  • Humans
  • Lipoproteins, LDL / metabolism
  • Macrophages / metabolism
  • Mice
  • Randomized Controlled Trials as Topic
  • Women's Health

Substances

  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Estrogens
  • HSP27 Heat-Shock Proteins
  • Lipoproteins, LDL