© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Innate immunity and cardiac preconditioning: a putative intrinsic cardioprotective program
Hatter Institute for Cardiology Research, MRC Inter-University Cape Heart Group, University of Cape Town Medical School, 7925 Cape Town, South Africa
* Corresponding author. Tel.: +27-21-406-6358; fax: +27-21-447-8789 sack{at}capeheart.uct.ac.za
Ischemic preconditioning is thought to evoke cell survival programs in the heart in large part via the activation of GI-protein coupled receptor signal transduction pathways. However, the identification and characterization of GI-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 TNF
, IL-1β 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 GI-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.
KEYWORDS Cytokines; Immunology; Ischemia; Preconditioning; Signal transduction
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
C. A. Petersen, K. A. Krumholz, J. Carmen, A. P. Sinai, and B. A. Burleigh Trypanosoma cruzi Infection and Nuclear Factor Kappa B Activation Prevent Apoptosis in Cardiac Cells Infect. Immun., March 1, 2006; 74(3): 1580 - 1587. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Lecour, N. Suleman, G. A. Deuchar, S. Somers, L. Lacerda, B. Huisamen, and L. H. Opie Pharmacological Preconditioning With Tumor Necrosis Factor-{alpha} Activates Signal Transducer and Activator of Transcription-3 at Reperfusion Without Involving Classic Prosurvival Kinases (Akt and Extracellular Signal-Regulated Kinase) Circulation, December 20, 2005; 112(25): 3911 - 3918. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. G. Neri Serneri, M. Boddi, P. A. Modesti, I. Cecioni, M. Coppo, M. L. Papa, T. Toscano, A. Marullo, and M. Chiavarelli Immunomediated and Ischemia-Independent Inflammation of Coronary Microvessels in Unstable Angina Circ. Res., June 27, 2003; 92(12): 1359 - 1366. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Vaage and G. Valen Preconditioning and cardiac surgery Ann. Thorac. Surg., February 1, 2003; 75(2): S709 - 714. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Martire, B. Fernandez, A. Buehler, C. Strohm, J. Schaper, R. Zimmermann, P. E Kolattukudy, and W. Schaper Cardiac overexpression of monocyte chemoattractant protein-1 in transgenic mice mimics ischemic preconditioning through SAPK/JNK1/2 activation Cardiovasc Res, February 1, 2003; 57(2): 523 - 534. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. M Yellon and J. M Downey Spotlight on preconditioning Cardiovasc Res, August 15, 2002; 55(3): 425 - 428. [Full Text] [PDF] |
||||




