The DOI matches its Crossref record; 237 of the 237 references it cites were found in a registry or an index.
Mitochondrial Metabolism in Aging Heart
Open accessAbstract
Altered mitochondrial metabolism is the underlying basis for the increased sensitivity in the aged heart to stress. The aged heart exhibits impaired metabolic flexibility, with a decreased capacity to oxidize fatty acids and enhanced dependence on glucose metabolism. Aging impairs mitochondrial oxidative phosphorylation, with a greater role played by the mitochondria located between the myofibrils, the interfibrillar mitochondria. With aging, there is a decrease in activity of complexes III and IV, which account for the decrease in respiration. Furthermore, aging decreases mitochondrial content among the myofibrils. The end result is that in the interfibrillar area, there is ≈50% decrease in mitochondrial function, affecting all substrates. The defective mitochondria persist in the aged heart, leading to enhanced oxidant production and oxidative injury and the activation of oxidant signaling for cell death. Aging defects in mitochondria represent new therapeutic targets, whether by manipulation of the mitochondrial proteome, modulation of electron transport, activation of biogenesis or mitophagy, or the regulation of mitochondrial fission and fusion. These mechanisms provide new ways to attenuate cardiac disease in elders by preemptive treatment of age-related defects, in contrast to the treatment of disease-induced dysfunction.
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Citations
Cites
1 retracted
Age related changes in NAD+ metabolism oxidative stress and Sirt1 activity in wistar rats
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Cited by
Mitochondrial function as a therapeutic target in heart failure
Brown, D. A., Perry, J. B., Allen, M. E., Sabbah, H. N., Stauffer, B. L., Shaikh, S. R., Cleland, J. G. F., Colucci, W. S., Butler, J., Voors, A. A., et al. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2016.203 · Cited by 803
Age-related changes in glucose metabolism, hyperglycemia, and cardiovascular risk
Chia, C. W., Egan, J. M., & Ferrucci, L. (2018) · Circulation Research · doi:10.1161/circresaha.118.312806 · Cited by 454
Autophagy in Cardiovascular Aging
Abdellatif, M., Sedej, S., Carmona-Gutierrez, D., Madeo, F., & Kroemer, G. (2018) · Circulation Research · doi:10.1161/circresaha.118.312208 · Cited by 239
Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte
Zhang, H., Alder, N. N., Wang, W., Szeto, H., Marcinek, D. J., & Rabinovitch, P. S. (2020) · eLife · doi:10.7554/elife.60827 · Cited by 101
Ruiz-Meana, M., Bou-Teen, D., Ferdinandy, P., Gyongyosi, M., Pesce, M., Perrino, C., Schulz, R., Sluijter, J. P. G., Tocchetti, C. G., Thum, T., et al. (2020) · Cardiovascular Research · doi:10.1093/cvr/cvaa132 · Cited by 67
Metadata
- Authors
- Lesnefsky, E. J., Chen, Q., & Hoppel, C. L.
- Venue
- Circulation Research
- Published
- 2016-05-13
- Volume
- 118
- Issue
- 10
- Pages
- 1593-1611
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2360592203
- Cited by
- 353
- References
- 237
- FWCI
- 11.74
- Type
- journal article
- Language
- en
- Open access
- bronze
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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).
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