Corruption of coronary collateral growth in metabolic syndrome: Role of oxidative stress.

Corruption of coronary collateral growth in metabolic syndrome: Role of oxidative stress.

Pung Yuh Fen; Chilian William M

World journal of cardiology

2010

2010-12

The myocardium adapts to ischemic insults in a variety of ways. One adaptation is the phenomenon of acute preconditioning, which can greatly ameliorate ischemic damage. However, this effect wanes within a few hours and does not confer chronic protection. A more chronic adaptation is the so-called second window of preconditioning, which enables protection for a few days. The most potent adaptation invoked by the myocardium to minimize the effects of ischemia is the growth of blood vessels in the heart, angiogenesis and arteriogenesis (collateral growth), which prevent the development of ischemia by enabling flow to a jeopardized region of the heart. This brief review examines the mechanisms underlying angiogenesis and arteriogenesis in the heart. The concept of a redox window, which is an optimal redox state for vascular growth, is discussed along with signaling mechanisms invoked by reactive oxygen species that are stimulated during ischemia-reperfusion. Finally, the review discusses of some of the pathologies, especially the metabolic syndrome, that negatively affect collateral growth through the corruption of redox signaling processes.

Angiogenesis; Mitochondria; Arteriogenesis; Redox-dependent signaling

Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).

421–427

12

2