Autophagy in cardiovascular biology
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Cardiovascular disease is the leading cause of death worldwide. As such, there is great interest in identifying novel mechanisms that govern the cardiovascular response to disease-related stress. First described in failing hearts, autophagy within the cardiovascular system has been widely characterized in cardiomyocytes, cardiac fibroblasts, endothelial cells, vascular smooth muscle cells, and macrophages. In all cases, a window of optimal autophagic activity appears to be critical to the maintenance of cardiovascular homeostasis and function; excessive or insufficient levels of autophagic flux can each contribute to heart disease pathogenesis. In this Review, we discuss the potential for targeting autophagy therapeutically and our vision for where this exciting biology may lead in the future.
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This work was supported by funds from the NIH (grants HL-120732, HL-100401, and HL-097768), American Heart Association Strategically Focused Research Network (14SFRN20740000), Cancer Prevention Research Institute of Texas (grant RP110486P3), Leducq Foundation (grant 11CVD04), and Comision Nacional de Investigacion Cientifica y Tecnologica de Chile (FONDAP grant 15130011 to S. Lavandero and M. Chiong, Redes grant 120003 to S. Lavandero and J.A. Hill, ACT grant 1111 to S. Lavandero and M. Chiong, FONDECYT grants 1120212 to S. Lavandero and 1140329 to M. Chiong).
Quote ItemThe Journal of Clinical Investigation. 2015;125(1):55–64
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