The DOI matches its Crossref record; 74 of the 74 references it cites were found in a registry or an index.
Inflammatory, Metabolic, and Genetic Mechanisms of Vascular Calcification
Open accessAbstract
This review centers on updating the active research area of vascular calcification. This pathology underlies substantial cardiovascular morbidity and mortality, through adverse mechanical effects on vascular compliance, vasomotion, and, most likely, plaque stability. Biomineralization is a complex, regulated process occurring widely throughout nature. Decades ago, its presence in the vasculature was considered a mere curiosity and an unregulated, dystrophic process that does not involve biological mechanisms. Although it remains controversial whether the process has any adaptive value or past evolutionary advantage, substantial advances have been made in understanding the biological mechanisms driving the process. Different types of calcific vasculopathy, such as inflammatory versus metabolic, have parallel mechanisms in skeletal bone calcification, such as intramembranous and endochondral ossification. Recent work has identified important regulatory roles for inflammation, oxidized lipids, elastin, alkaline phosphatase, osteoprogenitor cells, matrix γ-carboxyglutamic acid protein, transglutaminase, osteoclastic regulatory factors, phosphate regulatory hormones and receptors, apoptosis, prelamin A, autophagy, and microvesicles or microparticles similar to the matrix vesicles of skeletal bone. Recent work has uncovered fascinating interactions between matrix γ-carboxyglutamic acid protein, vitamin K, warfarin, and transport proteins. And, lastly, recent breakthroughs in inherited forms of calcific vasculopathy have identified the genes responsible as well as an unexpected overlap of phenotypes. Until recently, vascular calcification was considered a purely degenerative, unregulated process. Since then, investigative groups around the world have identified a wide range of causative mechanisms and regulatory pathways, and some of the recent developments are highlighted in this review.
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Cites
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Cited by
Yahagi, K., Kolodgie, F. D., Lutter, C., Mori, H., Romero, M. E., Finn, A. V., & Virmani, R. (2017) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.116.306256 · Cited by 573
Vascular calcification: Mechanisms of vascular smooth muscle cell calcification
Leopold, J. A. (2015) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2014.10.021 · Cited by 468
Vascular Calcification—New Insights into Its Mechanism
Lee, S. J., Lee, I.-K., & Jeon, J.-H. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21082685 · Cited by 438
Calcium deposition within coronary atherosclerotic lesion: Implications for plaque stability
Jinnouchi, H., Sato, Y., Sakamoto, A., Cornelissen, A., Mori, M., Kawakami, R., Gadhoke, N. V., Kolodgie, F. D., Virmani, R., & Finn, A. V. (2020) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2020.05.017 · Cited by 195
Metadata
- Authors
- Demer, L. L., & Tintut, Y.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2014-04
- Volume
- 34
- Issue
- 4
- Pages
- 715-723
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2152713621
- Cited by
- 353
- References
- 74
- FWCI
- 20.21
- Type
- journal article
- Language
- en
- Open access
- bronze
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