Endogenous IRAK-M Attenuates Postinfarction Remodeling Through Effects on Macrophages and Fibroblasts | Zendy

Wei Chen | Zendy; Amit Saxena | Zendy; Na Li | Zendy; Jin-Yu Sun | Zendy; Amit Gupta | Zendy; Dong-Wook Lee | Zendy; Qi Tian | Zendy; Marcin Dobaczewski | Zendy; Nikolaos G. Frangogiannis | Zendy

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Endogenous IRAK-M Attenuates Postinfarction Remodeling Through Effects on Macrophages and Fibroblasts

Author(s) -

Wei Chen,

Amit Saxena,

Na Li,

Jin-Yu Sun,

Amit Gupta,

Dong-Wook Lee,

Qi Tian,

Marcin Dobaczewski,

Nikolaos G. Frangogiannis

Publication year - 2012

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.112.300310

Subject(s) - inflammation , proinflammatory cytokine , ventricular remodeling , fibroblast , medicine , downregulation and upregulation , innate immune system , immune system , cytokine , receptor , immunology , microbiology and biotechnology , biology , myocardial infarction , in vitro , biochemistry , gene

Effective postinfarction repair requires timely suppression of innate immune signals to prevent the catastrophic consequences of uncontrolled inflammation on cardiac geometry and function. In macrophages, interleukin-1 receptor-associated kinase (IRAK)-M acts as a functional decoy preventing uncontrolled toll-like receptor /interleukin-1-mediated responses. Our study investigates the role of IRAK-M as a negative regulator of the postinfarction inflammatory response and as a modulator of cardiac remodeling.

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