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- W2200501315 abstract "Myeloid-derived growth factor (C19orf10) mediates cardiac repair following myocardial infarction Korf-Klingebiel et alNat Med . 2015;21:140–149.In the infarcted myocardium, cardiomyocyte necrosis activates inflammatory cascades resulting in recruitment of myeloid cells that have been suggested to extend ischemic injury, but also clear the infarct from dead cells and matrix debris, and stimulate the reparative process. A growing body of evidence suggests that subsets of myeloid cells may exert protective actions on the infarcted myocardium. A recently published study in Nature Medicine , identified myeloid-derived growth factor as an antiapoptotic and angiogenic mediator that is secreted by a subset of macrophages and may protect the infarcted heart from adverse remodeling. The adult mammalian heart has negligible regenerative capacity. Cardiomyocyte necrosis triggers an intense inflammatory reaction leading to the formation of a collagen-based scar.1 The infarcted myocardium is rapidly infiltrated with abundant myeloid cells, which are primarily localized in the border zone and interact with viable cardiomyocytes. Over the past 3 decades, researchers have struggled to identify detrimental and protective inflammatory signals, to design therapeutic strategies for patients with myocardial infarction. A large body of experimental evidence suggested that neutrophils and proinflammatory monocytes may extend ischemic injury, inducing cytotoxic effects on surviving cardiomyocytes and promoting extracellular matrix degradation.1 In experimental models, targeted inhibition of β2 integrins to disrupt the adhesive cascade that mediates neutrophil recruitment in the infarct showed great promise, reducing infarct size in rodent, canine and primate models of myocardial infarction.2 Unfortunately, in human patients, 3 small clinical trials targeting β2 integrins failed to reduce infarct size.3More recently, several studies have focused on the protective actions of leukocyte subpopulations. In experimental models, cell therapy with bone marrow mononuclear cells enhanced function of the infarcted heart.4 These observations suggested that myeloid cell subsets secrete …" @default.
- W2200501315 created "2016-06-24" @default.
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- W2200501315 date "2015-06-19" @default.
- W2200501315 modified "2023-09-25" @default.
- W2200501315 title "Mediators Secreted by Myeloid Cells May Protect and Repair the Infarcted Myocardium" @default.
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- W2200501315 doi "https://doi.org/10.1161/circresaha.115.306283" @default.
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