Journal
TRANSLATIONAL RESEARCH
Volume 167, Issue 1, Pages 152-166Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.trsl.2015.07.002
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Funding
- National Institutes of Health [R01 HL76246, R01 HL85440]
- Fondazione Cassa di Risparmio di Lucca
- Fondazione Banca del Monte di Lucca
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL085440, R01HL076246] Funding Source: NIH RePORTER
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In the infarcted myocardium, necrotic cardiomyocytes release danger signals, activating an intense inflammatory response. Inflammatory pathways play a crucial role in regulation of a wide range of cellular processes involved in injury, repair, and remodeling of the infarcted heart. Proinflammatory cytokines, such as tumor necrosis factor alpha and interleukin 1, are markedly upregulated in the infarcted myocardium and promote adhesive interactions between endothelial cells and leukocytes by stimulating chemokine and adhesion molecule expression. Distinct pairs of chemokines and chemokine receptors are implicated in recruitment of various leukocyte subpopulations in the infarcted myocardium. For more than the past 30 years, extensive experimental work has explored the role of inflammatory signals and the contributions of leukocyte subpopulations in myocardial infarction. Robust evidence derived from experimental models of myocardial infarction has identified inflammatory targets that may attenuate cardiomyocyte injury or protect from adverse remodeling. Unfortunately, attempts to translate the promising experimental findings to clinical therapy have failed. This review article discusses the biology of the inflammatory response after myocardial infarction, attempts to identify the causes for the translational failures of the past, and proposes promising new therapeutic directions. Because of their potential involvement in injurious, reparative, and regenerative responses, inflammatory cells may hold the key for design of new therapies in myocardial infarction.
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