The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Mitochondrial DNA Damage Can Promote Atherosclerosis Independently of Reactive Oxygen Species Through Effects on Smooth Muscle Cells and Monocytes and Correlates With Higher-Risk Plaques in Humans
Open accessAbstract
Background—: Mitochondrial DNA (mtDNA) damage occurs in both circulating cells and the vessel wall in human atherosclerosis. However, it is unclear whether mtDNA damage directly promotes atherogenesis or is a consequence of tissue damage, which cell types are involved, and whether its effects are mediated only through reactive oxygen species. Methods and Results—: mtDNA damage occurred early in the vessel wall in apolipoprotein E–null (ApoE −/− ) mice, before significant atherosclerosis developed. mtDNA defects were also identified in circulating monocytes and liver and were associated with mitochondrial dysfunction. To determine whether mtDNA damage directly promotes atherosclerosis, we studied ApoE −/− mice deficient for mitochondrial polymerase-γ proofreading activity (polG −/− /ApoE −/− ). polG −/− /ApoE −/− mice showed extensive mtDNA damage and defects in oxidative phosphorylation but no increase in reactive oxygen species. polG −/− /ApoE −/− mice showed increased atherosclerosis, associated with impaired proliferation and apoptosis of vascular smooth muscle cells, and hyperlipidemia. Transplantation with polG −/− /ApoE −/− bone marrow increased the features of plaque vulnerability, and polG −/− /ApoE −/− monocytes showed increased apoptosis and inflammatory cytokine release. To examine mtDNA damage in human atherosclerosis, we assessed mtDNA adducts in plaques and in leukocytes from patients who had undergone virtual histology intravascular ultrasound characterization of coronary plaques. Human atherosclerotic plaques showed increased mtDNA damage compared with normal vessels; in contrast, leukocyte mtDNA damage was associated with higher-risk plaques but not plaque burden. Conclusions—: We show that mtDNA damage in vessel wall and circulating cells is widespread and causative and indicates higher risk in atherosclerosis. Protection against mtDNA damage and improvement of mitochondrial function are potential areas for new therapeutics.
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Cites
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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
Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease
Lacolley, P., Regnault, V., Segers, P., & Laurent, S. (2017) · Physiological Reviews · doi:10.1152/physrev.00003.2017 · Cited by 734
Vascular Smooth Muscle Cell Senescence Promotes Atherosclerosis and Features of Plaque Vulnerability
Wang, J., Uryga, A. K., Reinhold, J., Figg, N., Baker, L., Finigan, A., Gray, K., Kumar, S., Clarke, M., & Bennett, M. (2015) · Circulation · doi:10.1161/circulationaha.115.016457 · Cited by 349
Self-citationMitochondria, Oxidative Stress and Innate Immunity
Chen, Y., Zhou, Z., & Min, W. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.01487 · Cited by 315
Association of mitochondrial DNA copy number with cardiovascular disease
Ashar, F. N., Zhang, Y., Longchamps, R. J., Lane, J., Moes, A., Grove, M. L., Mychaleckyj, J. C., Taylor, K. D., Coresh, J., Rotter, J. I., et al. (2017) · JAMA Cardiology · doi:10.1001/jamacardio.2017.3683 · Cited by 295
Metadata
- Authors
- Yu, E., Calvert, P. A., Mercer, J. R., Harrison, J., Baker, L., Figg, N. L., Kumar, S., Wang, J. C., Hurst, L. A., Obaid, D. R., Logan, A., West, N. E. J., Clarke, M. C. H., Vidal-Puig, A., Murphy, M. P., & Bennett, M. R.
- Venue
- Circulation
- Published
- 2013-08-13
- Volume
- 128
- Issue
- 7
- Pages
- 702-712
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2113495231
- Cited by
- 283
- References
- 11
- FWCI
- 7.67
- Type
- journal article
- Language
- en
- Open access
- green
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- Yu, E., Calvert, P. A., Mercer, J. R., Harrison, J., Baker, L., Figg, N. L., Kumar, S., Wang, J. C., Hurst, L. A., Obaid, D. R., Logan, A., West, N. E. J., Clarke, M. C. H., Vidal-Puig, A., Murphy, M. P., & Bennett, M. R. (2013). Mitochondrial DNA Damage Can Promote Atherosclerosis Independently of Reactive Oxygen Species Through Effects on Smooth Muscle Cells and Monocytes and Correlates With Higher-Risk Plaques in Humans. Circulation. https://doi.org/10.1161/circulationaha.113.002271
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