Molecular mechanisms of autophagy in the cardiovascular system
Author
dc.contributor.author
Gatica, Damián
Author
dc.contributor.author
Chiong Lay, Mario
Author
dc.contributor.author
Lavandero González, Sergio
Author
dc.contributor.author
Klionsky, Daniel J.
Admission date
dc.date.accessioned
2019-03-18T11:52:31Z
Available date
dc.date.available
2019-03-18T11:52:31Z
Publication date
dc.date.issued
2015
Cita de ítem
dc.identifier.citation
Circ Res. 2015 January 30; 116(3): 456–467
Identifier
dc.identifier.issn
15244571
Identifier
dc.identifier.issn
00097330
Identifier
dc.identifier.other
10.1161/CIRCRESAHA.114.303788
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/166534
Abstract
dc.description.abstract
Autophagy is a catabolic recycling pathway triggered by various intra- or extracellular stimuli that
is conserved from yeast to mammals. During autophagy diverse cytosolic constituents are
enveloped by double-membrane vesicles, autophagosomes, which later fuse with lysosomes or the
vacuole in order to degrade their cargo. Dysregulation in autophagy is associated with a diverse
range of pathologies including cardiovascular disease, the leading cause of death in the world. 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 and vascular smooth muscle cells. 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. Here we review the molecular mechanisms that govern autophagosome formation
and analyze the link between autophagy and cardiovascular disease.