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In this study, a genetic mouse model with a chronic increase in VEGF\u2010A in the heart is shown to have increased cardiac angiogenesis and develop cardiac hypertrophy with enhanced basal cardiac performance with age progression. However, in aged hearts, this increase in VEGF\u2010A was associated with higher expression of fetal cardiac genes and reduced cardiac performance after p\u2010agonistic stress, features consistent with pathologic cardiac hypertrophy. Expression of Nod\u2010like receptor protein (NLRP)\u20103 was increased in the hearts of the mice, and its genetic inactivation prevented increased fetal cardiac gene expression and partially rescued the impaired cardiac performance after p\u2010agonistic stimulation in aged hearts without reducing cardiac angiogenesis or hypertrophy. Thus, although a chronic increase in cardiac VEGF\u2010A may improve cardiac perfusion, long\u2010term upregulation of VEGF\u2010A leads to reduced cardiac performance under stress, an effect that can be partially inhibited by NLRP3 inactivation. Targeting NLRP3 shifts the VEGF\u2010A\u2010induced cardiac hypertrophy from a pathologic toward a more physiologic hypertrophy.\u2014Marneros, A. G. Effects of chronically increased VEGF\u2010A on the aging heart. 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