Abstract
Cardiac repair following myocardial infarction is dependent on an inflammatory reaction and is closely intertwined with alterations in ventricular size and shape, termed ventricular remodeling. Aging has been associated with delayed wound healing and altered cellular responses to inflammatory and fibrogenic mediators. We examined the effects of aging on infarct healing and post-infarction remodeling using a model of reperfused murine myocardial infarction. Senescent mice (age>24 months) had increased infarct-related mortality, worse ventricular function and enhanced post-infarction remodeling (LVEDD 4.22±0.107mm vs 3.74±0.068mm p<0.001) than young (age 2–3 months) animals. Senescent mice showed impaired phagocytosis of dead cardiomyocytes, decreased and delayed inflammatory leukocyte infiltration in comparison with young mice. Senescence was associated with reduced myofibroblast density (p<0.0001) in the infarcted area and significantly lower collagen content in the scar (p<0.001). Aging is associated with a suppressed and prolonged inflammatory response resulting in decreased myofibroblast infiltration and collagen deposition in the infarct. Reduction in collagen content of the scar may decrease tensile strength, enhancing adverse remodeling.
Published Version
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