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- W2800905301 abstract "Significance Pressure overload triggers responses in cardiomyocytes and noncardiomyocytes, leading to pressure overload hypertrophy (POH). Here, we show that cardiac resident macrophages regulate compensatory myocardial adaptation to POH, while nonresident infiltrating macrophages are detrimental. At early-phase POH, pressure overload induces cardiac resident macrophage proliferation, which is regulated by Kruppel-like factor 4. At late-phase POH, pressure overload also induces Ly6C hi monocyte infiltration, and its blockade improves myocardial angiogenesis and preserves cardiac function. Mechanistically, the differential impact of these two macrophage subsets on myocardial angiogenesis may underlie the cardiac phenotype. These findings provide insights regarding the role of cardiac resident and nonresident macrophages, conceptually update the view of myocardial angiogenesis, and identify monocyte infiltration as a therapeutic target for nonischemic cardiomyopathy." @default.
- W2800905301 created "2018-05-17" @default.
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- W2800905301 date "2018-04-30" @default.
- W2800905301 modified "2023-10-17" @default.
- W2800905301 title "Distinct roles of resident and nonresident macrophages in nonischemic cardiomyopathy" @default.
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- W2800905301 doi "https://doi.org/10.1073/pnas.1720065115" @default.
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