Innate immunity and cardiac preconditioning: a putative intrinsic cardioprotective program

Cardiovasc Res. 2002 Aug 15;55(3):474-82. doi: 10.1016/s0008-6363(02)00288-2.

Abstract

Ischemic preconditioning is thought to evoke cell survival programs in the heart in large part via the activation of G(I)-protein coupled receptor signal transduction pathways. However, the identification and characterization of G(I)-protein coupled receptor independent pathways would enable researchers to pursue novel cellular events that could direct or promote preconditioning. In this regard recent work has begun to explore the role of the innate immune system in intrinsic cardioprotection against both viral myocarditis and ischemia. Interestingly, cytokines such as TNFalpha, IL-1beta and leukemia inhibitory factor, which are components of innate immunity, have been shown to mimic ischemic preconditioning. Thus as the innate immune system functions via a diverse array of G(I)-protein independent receptors, the study of this immunological system in the heart may provide new insight into mechanisms driving and promoting ischemic preconditioning. We propose that innate immunity is indeed an integral part of ischemic preconditioning. In this review, we provide an overview of the innate immune system, describe the studies whereby cytokines mimic ischemic preconditioning and finally postulate some mechanisms whereby innate immunity may promote cardioprotection as a component of preconditioning.

Publication types

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

MeSH terms

  • Animals
  • Cytokines / physiology*
  • Drosophila Proteins*
  • Humans
  • Immune Tolerance
  • Ischemic Preconditioning, Myocardial*
  • Lipopolysaccharides / pharmacology
  • Membrane Glycoproteins / metabolism
  • Models, Animal
  • Myocardial Ischemia / immunology*
  • Myocardium / immunology*
  • Receptors, Cell Surface / metabolism
  • Signal Transduction / physiology*
  • Time Factors
  • Toll-Like Receptors

Substances

  • Cytokines
  • Drosophila Proteins
  • Lipopolysaccharides
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • Toll-Like Receptors