Conditioning the whole heart-not just the cardiomyocyte

被引:51
作者
Bell, Robert M. [1 ]
Yellon, Derek M. [1 ]
机构
[1] Univ Coll London Hosp & Med Sch, Hatter Cardiovasc Inst, Inst Cardiovasc Sci, London WC1E 6HX, England
关键词
Preconditioning; Remote conditioning; Postconditioning; Cardiac myocyte; Endothelium; Fibroblast; NITRIC-OXIDE SYNTHASE; ISCHEMIA-REPERFUSION INJURY; FIBROBLAST GROWTH FACTOR-2; ADULT MAMMALIAN HEART; KALLIDIN-LIKE PEPTIDE; MYOCARDIAL-ISCHEMIA; REFLOW PHENOMENON; HEME OXYGENASE-1; METABOLIC INHIBITION; CARDIAC MYOCYTES;
D O I
10.1016/j.yjmcc.2012.04.001
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Conditioning, the recruitment of endogenous cytoprotective pathways that protect the myocardium against injurious ischaemia/reperfusion injury, has developed into a range of modalities that can be applied before (preconditioning), during (perconditioning) or after the injurious ischaemic insult (postconditioning), either directly to the heart or in a distal tissue (remote preconditioning). A wide range of triggers, signaling pathways and potential end-effector mechanisms have been identified, which appear common to all forms of conditioning. Interestingly, conditioning applies to not only the cardiac myocyte, but to all the constitutive cell types within the myocardium. As our understanding of conditioning mechanisms continue to develop and we start to realise some of the difficulties in translating these phenomena to clinical treatments, it may be time to take a more integrative approach to conditioning, considering the many cellular and tissue types within the heart, and how they contribute to cytoprotective adaptations. In this review, we shall look at the conditioning phenomena, how different cell types contribute to the conditioned phenotype, and where novel cardioprotective modalities may be developed. (c) 2012 Published by Elsevier Ltd.
引用
收藏
页码:24 / 32
页数:9
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