Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 125, Issue 8, Pages 2927-2930Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI83191
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL085440, R01HL076246] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL76246, R01 HL085440, R01 HL076246, R01 HL85440] Funding Source: Medline
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The mammalian heart contains a population of resident macrophages that expands in response to myocardial infarction through the recruitment of monocytes. Infarct macrophages exhibit high phenotypic diversity and respond to microenvironmental cues by altering their functional properties and secretory profile. In this issue of the JCI, de Couto and colleagues demonstrate that infiltrating macrophages can be primed to acquire a cardioprotective phenotype in ischemic heart and exert this proactive effect through activation of an antiapoptotic program in cardiomyocytes. This study supports the growing body of evidence that suggests that macrophage subpopulations can be modulated to mediate cytoprotective, reparative, and even regenerative functions in the infarcted heart. The cellular Mechanisms and molecular signals driving these macrophage phenotypes are yet unknown; however, harnessing the remarkable potential of the macrophage in regulating cell survival and tissue regeneration may hold therapeutic promise for myocardial infarction.
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