Abstract

The adult mammalian heart contains a large number of pericytes that regulate blood flow, while supporting baseline microvascular structure and function. Considering their abundance, strategic peri-endothelial location, functional diversity and phenotypic plasticity, pericytes may be critically involved in a wide range of myocardial pathologic conditions. Following myocardial infarction, cardiac pericytes may regulate inflammatory, reparative, angiogenic and fibrogenic responses. Moreover, pericyte-mediated microvascular constriction may contribute to the pathogenesis of “no-reflow” in the ischemic and reperfused myocardium. Cell therapy with pericytes has been suggested to exert beneficial actions in experimental models of myocardial infarction. The underlying mechanisms of protection may involve modulation of inflammation, suppression of fibrosis and stimulation of angiogenesis. Pericytes may also be involved in the pathogenesis of heart failure by converting to myofibroblasts, by secreting fibrogenic and pro-inflammatory mediators, and my regulating microvascular blood flow. Unfortunately, limited information is currently available on the role of pericytes in myocardial diseases. There is an urgent need for systematic investigation of pericyte actions in the ischemic, infarcted and failing heart using experimental animal models and human studies.

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