Oxidative stress and autophagy in cardiovascular homeostasis
Author
dc.contributor.author
Morales, Cyndi R.
Author
dc.contributor.author
Pedrozo Cibils, Zully
Author
dc.contributor.author
Lavandero González, Sergio
Author
dc.contributor.author
Hill, Joseph A.
Admission date
dc.date.accessioned
2019-01-29T13:56:14Z
Available date
dc.date.available
2019-01-29T13:56:14Z
Publication date
dc.date.issued
2014
Cita de ítem
dc.identifier.citation
Antioxidants and Redox Signaling, Volume 20, Number 3, 2014
Identifier
dc.identifier.issn
15230864
Identifier
dc.identifier.issn
15577716
Identifier
dc.identifier.other
10.1089/ars.2013.5359
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/160099
Abstract
dc.description.abstract
Significance: Autophagy is an evolutionarily ancient process of intracellular protein and organelle recycling required to maintain cellular homeostasis in the face of a wide variety of stresses. Dysregulation of reactive oxygen
species (ROS) and reactive nitrogen species (RNS) leads to oxidative damage. Both autophagy and ROS/RNS serve
pathological or adaptive roles within cardiomyocytes, depending on the context. Recent Advances: ROS/RNS and
autophagy communicate with each other via both transcriptional and post-translational events. This cross talk, in
turn, regulates the structural integrity of cardiomyocytes, promotes proteostasis, and reduces inflammation, events
critical to disease pathogenesis. Critical Issues: Dysregulation of either autophagy or redox state has been implicated in many cardiovascular diseases. Cardiomyocytes are rich in mitochondria, which make them particularly
sensitive to oxidative damage. Maintenance of mitochondrial homeostasis and elimination of defective mitochondria are each critical to the maintenance of redox homeostasis. Future Directions: The complex interplay
between autophagy and oxidative stress underlies a wide range of physiological and pathological events and its
elucidation holds promise of potential clinical applicability.