The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Integration of cellular bioenergetics with mitochondrial quality control and autophagy
Open accessAbstract
Bioenergetic dysfunction is emerging as a cornerstone for establishing a framework for understanding the pathophysiology of cardiovascular disease, diabetes, cancer and neurodegeneration. Recent advances in cellular bioenergetics have shown that many cells maintain a substantial bioenergetic reserve capacity, which is a prospective index of ‘healthy’ mitochondrial populations. The bioenergetics of the cell are likely regulated by energy requirements and substrate availability. Additionally, the overall quality of the mitochondrial population and the relative abundance of mitochondria in cells and tissues also impinge on overall bioenergetic capacity and resistance to stress. Because mitochondria are susceptible to damage mediated by reactive oxygen/nitrogen and lipid species, maintaining a ‘healthy’ population of mitochondria through quality control mechanisms appears to be essential for cell survival under conditions of pathological stress. Accumulating evidence suggest that mitophagy is particularly important for preventing amplification of initial oxidative insults, which otherwise would further impair the respiratory chain or promote mutations in mitochondrial DNA (mtDNA). The processes underlying the regulation of mitophagy depend on several factors, including the integrity of mtDNA, electron transport chain activity, and the interaction and regulation of the autophagic machinery. The integration and interpretation of cellular bioenergetics in the context of mitochondrial quality control and genetics is the theme of this review.
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Cites
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PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
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PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
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Metformin reverses established lung fibrosis in a bleomycin model
Rangarajan, S., Bone, N. B., Zmijewska, A. A., Jiang, S., Park, D. W., Bernard, K., Locy, M. L., Ravi, S., Deshane, J., Mannon, R. B., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0087-6 · Cited by 560
Self-citationMitochondria and Endothelial Function
Kluge, M. A., Fetterman, J. L., & Vita, J. A. (2013) · Circulation Research · doi:10.1161/circresaha.111.300233 · Cited by 508
Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View
Cenini, G., Lloret, A., & Cascella, R. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/2105607 · Cited by 499
p38 signaling inhibits mTORC1-independent autophagy in senescent human CD8+ T cells
Henson, S. M., Lanna, A., Riddell, N. E., Franzese, O., Macaulay, R., Griffiths, S. J., Puleston, D. J., Watson, A. S., Simon, A. K., Tooze, S. A., et al. (2014) · Journal of Clinical Investigation · doi:10.1172/jci75051 · Cited by 389
Cellular metabolic and autophagic pathways: Traffic control by redox signaling
Dodson, M., Darley-Usmar, V., & Zhang, J. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.05.014 · Cited by 324
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Metadata
- Authors
- Hill, B. G., Benavides, G. A., Lancaster, J. R., Ballinger, S., Dell’Italia, L., Zhang, J., & Darley-Usmar, V. M.
- Venue
- bchm
- Publisher
- Walter de Gruyter GmbH
- Published
- 2012-11-13
- Volume
- 393
- Issue
- 12
- Pages
- 1485-1512
- ISSN
- 1431-6730 (ISSN-L)
- 1437-4315
- OpenAlex
- W1978048781
- Cited by
- 490
- References
- 44
- FWCI
- 21.33
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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