The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Autophagy During Cardiac Stress: Joys and Frustrations of Autophagy
Open accessAbstract
The study of autophagy has been transformed by the cloning of most genes in the pathway and the introduction of GFP-LC3 as a reporter to allow visual assessment of autophagy. The field of cardiac biology is not alone in attempting to understand the implications of autophagy. The purpose of this review is to address some of the controversies and conundrums associated with the evolving studies of autophagy in the heart. Autophagy is a cellular process involving a complex orchestration of regulatory gene products as well as machinery for assembly, selective targeting, and degradation of autophagosomes and their contents. Our understanding of the role of autophagy in human disease is rapidly evolving as investigators examine the process in different tissues and different pathophysiological contexts. In the field of heart disease, autophagy has been examined in the settings of ischemia and reperfusion, preconditioning, cardiac hypertrophy, and heart failure. This review addresses the role of autophagy in cardioprotection, the balance of catabolism and anabolism, the concept of mitochondrial quality control, and the implications of impaired autophagic flux or frustrated autophagy.
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Cites
Rapamycin fed late in life extends lifespan in genetically heterogeneous mice
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Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
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“The mitochondrial quality-control hypothesis was first advanced by Shirihai’s group (67), who showed that mitochondrial fusion is followed by fission, resulting in two daughter mitochondria: one with high membrane potential that can proceed to successive rounds of fusion and fission and one with low membrane potential…”
BackgroundReactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4
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“Atg4 is redox regulated and appears to be responsible for upregulating autophagy in the face of oxidative stress (2).”
BackgroundSelective degradation of mitochondria by mitophagy
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Cited by
Rubinsztein, D. C., Mariño, G., & Kroemer, G. (2011) · Cell · doi:10.1016/j.cell.2011.07.030 · Cited by 2,107
Mitochondria and the Autophagy–Inflammation–Cell Death Axis in Organismal Aging
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The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy
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A review on the mechanisms of blood-flow restriction resistance training-induced muscle hypertrophy
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Metadata
- Authors
- Gottlieb, R. A., & Mentzer, R. M.
- Venue
- Annual Review of Physiology
- Publisher
- Annual Reviews
- Published
- 2010-03-17
- Volume
- 72
- Issue
- 1
- Pages
- 45-59
- ISSN
- 0066-4278 (ISSN-L)
- 1545-1585
- OpenAlex
- W2143397461
- Cited by
- 267
- References
- 12
- FWCI
- 2.83
- Type
- journal article
- Language
- en
- Open access
- green
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- Gottlieb, R. A., & Mentzer, R. M. (2010). Autophagy During Cardiac Stress: Joys and Frustrations of Autophagy. Annual Review of Physiology. https://doi.org/10.1146/annurev-physiol-021909-135757
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
