PDCD5 protects against cardiac remodeling by regulating autophagy and apoptosis.

Cardiac remodeling, including cardiac hypertrophy and fibrosis, is an important pathological process that can lead to heart failure. A previous study demonstrated that autophagy could represent an active adaptive response in cardiomyocytes that affords protection from cardiac remodeling. In the present study, we investigated the role of an autophagy-related gene, PDCD5 (Programmed cell death 5), in cardiac remodeling induced by β-adrenergic stimulation in vivo. We report for the first time that mice systemically overexpressing PDCD5 (PDCD5tg) were protected from cardiac remodeling. In addition, cardiac function was preserved in PDCD5tg mice in response to isoproterenol (ISO) stimulation. Importantly, basal autophagy was significantly higher in PDCD5tg mice than in the wild-type (WT) mice. Moreover, apoptosis was significantly lower in PDCD5tg mice than in WT mice, among the ISO-induced animals. In summary, our findings reveal that PDCD5 overexpression improves cardiac function and inhibits cardiac remodeling induced by ISO via induction of autophagy and inhibition of apoptosis.

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