The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Dysregulation of mitochondrial biogenesis in vascular endothelial and smooth muscle cells of aged rats
Abstract
Mitochondrial biogenesis is involved in the control of cell metabolism, signal transduction, and regulation of mitochondrial reactive oxygen species (ROS) production. Despite the central role of mitochondria in cellular aging and endothelial physiology, there are no studies extant investigating age-related alterations in mitochondrial biogenesis in blood vessels. Electronmicroscopy and confocal microscopy (en face Mitotracker staining) revealed that in aortas of F344 rats, a decline in mitochondrial biogenesis occurs with aging. In aged vessels, the expression of the mitochondrial biogenesis factors (including mitochondrial transcription factor A and peroxisome proliferator-activated receptor-γ coactivator-1) was decreased. The vascular expression of complex I, III, and IV significantly declined with age, whereas aging did not alter the expression of complex II and V. Cytochrome c oxidase (COX) expression/activity exhibited the greatest age-related decline, which was associated with increased mitochondrial ROS production in the aged vessels. In cultured coronary arterial endothelial cells, a partial knockdown of COX significantly increased mitochondrial ROS production. In conclusion, vascular aging is characterized by a decline in mitochondrial mass in the endothelial cells and an altered expression of components of the mitochondrial electron transport chain likely due to a dysregulation of mitochondrial biogenesis factors. We posit that impaired mitochondrial biogenesis and downregulation of COX may contribute to the increased mitochondrial oxidative stress in aged endothelial cells.
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Cites
Resveratrol improves health and survival of mice on a high-calorie diet
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Calorie restriction promotes mitochondrial biogenesis by inducing the expression of eNOS
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“Moreover, caloric restriction, which slows down metabolic activity, was shown to increase mitochondrial biogenesis (37).”
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Endothelial Nitric Oxide Synthase (eNOS) Knockout Mice Have Defective Mitochondrial β-Oxidation
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Cited by
Ungvari, Z., Tarantini, S., Donato, A. J., Galvan, V., & Csiszar, A. (2018) · Circulation Research · doi:10.1161/circresaha.118.311378 · Cited by 919
Self-citationMechanisms of Dysfunction in the Aging Vasculature and Role in Age-Related Disease
Donato, A. J., Machin, D. R., & Lesniewski, L. A. (2018) · Circulation Research · doi:10.1161/circresaha.118.312563 · Cited by 688
Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials
Marzetti, E., Calvani, R., Cesari, M., Buford, T. W., Lorenzi, M., Behnke, B. J., & Leeuwenburgh, C. (2013) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2013.06.024 · Cited by 627
Cellular and molecular biology of aging endothelial cells
Donato, A. J., Morgan, R. G., Walker, A. E., & Lesniewski, L. A. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.01.021 · Cited by 538
Mechanisms of Vascular Aging: New Perspectives
Ungvari, Z., Kaley, G., de Cabo, R., Sonntag, W. E., & Csiszar, A. (2010) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glq113 · Cited by 531
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Metadata
- Authors
- Ungvari, Z., Labinskyy, N., Gupte, S., Chander, P. N., Edwards, J. G., & Csiszar, A.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2008-05
- Volume
- 294
- Issue
- 5
- Pages
- H2121-H2128
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2106996966
- Cited by
- 200
- References
- 10
- FWCI
- 4.71
- Type
- journal article
- Language
- en
- Open access
- closed
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