Molecular Mechanisms of Autophagy in the Cardiovascular System
Open accessAbstract
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 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. Accordingly, there is tremendous interest in modulating autophagy for therapeutic purposes. One complexity with regard to cardiovascular homeostasis, however, is that the timing of autophagic activity appears to be critical; for example, cardiomyocyte autophagy during ischemia/reperfusion can be either beneficial or harmful. Here, we review the molecular mechanisms that govern autophagosome formation and analyze the link between autophagy and cardiovascular disease.
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Endogenous defects in autophagy are associated with embryonic lethality, developmental defects, and multiple pathological disorders including neurodegeneration, cancer, and cardiovascular disorders.
“and permanent or transient endogenous defects in autophagy have been associated with embryonic lethality, developmental defects, and multiple pathological disorders, including (but not limited to) neurodegeneration, cancer, and cardiovascular disorders [812–817].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [812]
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References 161 · Cited by 272
Research works printed but not linked: 1
- [106]World Health Organization Global health risks: Mortality and burden of disease attributable to selected major risks 2009 WHO Press
- Authors
- Gatica, D., Chiong, M., Lavandero, S., & Klionsky, D. J.
- Affiliations
- University of Michigan (US)
- Venue
- Circulation Research
- Published
- 2015-01-30
- Volume
- 116
- Issue
- 3
- Pages
- 456-467
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC4313620
- OpenAlex
- W2023680287
- Cited by
- 272
- References
- 161
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 17 · 2023: 19 · 2022: 28 · 2021: 29 · 2020: 28 · 2019: 28 · 2018: 37 · 2017: 22 · 2016: 29 · 2015: 12
- FWCI
- 4.34
- Type
- journal article
- Language
- en
- Update notices
- correction (2015-03-27)
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Universidad de Chile (submittedVersion, cc-by-nc-nd)
- Funders
- Universidad de Chile
- National Institute of General Medical Sciences (GM053396, R01GM053396)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- autophagy, autophagosome formation, cardiovascular disease, cardiomyocytes, cardiac fibroblasts, endothelial cells, vascular smooth muscle cells, autophagic flux, heart failure, cardiovascular homeostasis, lysosomal degradation
- MeSH terms
- Animals, Autophagy, Cardiovascular Diseases, Humans, Myocytes, Cardiac
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