Why the study?
Does blockade of blood-borne macrophage infiltration improve myocardial angiogenesis and preserve cardiac function in a pressure overload hypertrophy model of heart failure?
Population
Pressure overload hypertrophy (POH) model of heart failure representing nonischemic cardiomyopathy
Design
Preclinical
Authors
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Hypothesis-generating for macrophage-targeted therapy in pressure-overload HF; leaves open clinical translation pending human studies.
Does blockade of blood-borne macrophage infiltration improve myocardial angiogenesis and preserve cardiac function in a pressure overload hypertrophy model of heart failure?
This study demonstrates distinct temporal and spatial roles for resident and nonresident macrophages in heart failure development, identifying late-phase recruited macrophages as detrimental and a potential therapeutic target.
Liao et al. (2018) studied this question.
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