Molecular Mechanisms of Vascular Health: Insights From Vascular Aging and Calcification

Nadia R. Sutton; Rajeev Malhotra; Cynthia St. Hilaire; Elena Aikawa; Roger S. Blumenthal; Grace Gackenbach; Parag Goyal; Adam Johnson; Sagar U. Nigwekar; Catherine M. Shanahan; Dwight A. Towler; Brooke N. Wolford; Yabing Chen

doi:10.1161/ATVBAHA.122.317332

Molecular Mechanisms of Vascular Health: Insights From Vascular Aging and Calcification

Nadia R. Sutton, Rajeev Malhotra, Cynthia St. Hilaire, Elena Aikawa, Roger S. Blumenthal, Grace Gackenbach, Parag Goyal, Adam Johnson, Sagar U. Nigwekar, Catherine M. Shanahan, Dwight A. Towler, Brooke N. Wolford, Yabing Chen^*

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

58 Citations (Scopus)

Abstract

Cardiovascular disease is the most common cause of death worldwide, especially beyond the age of 65 years, with the vast majority of morbidity and mortality due to myocardial infarction and stroke. Vascular pathology stems from a combination of genetic risk, environmental factors, and the biologic changes associated with aging. The pathogenesis underlying the development of vascular aging, and vascular calcification with aging, in particular, is still not fully understood. Accumulating data suggests that genetic risk, likely compounded by epigenetic modifications, environmental factors, including diabetes and chronic kidney disease, and the plasticity of vascular smooth muscle cells to acquire an osteogenic phenotype are major determinants of age-associated vascular calcification. Understanding the molecular mechanisms underlying genetic and modifiable risk factors in regulating age-associated vascular pathology may inspire strategies to promote healthy vascular aging. This article summarizes current knowledge of concepts and mechanisms of age-associated vascular disease, with an emphasis on vascular calcification.

Original language	English
Pages (from-to)	15-29
Number of pages	15
Journal	Arteriosclerosis, Thrombosis, and Vascular Biology
Volume	43
Issue number	1
Early online date	22 Nov 2022
DOIs	https://doi.org/10.1161/ATVBAHA.122.317332
Publication status	Published - 1 Jan 2023

Keywords

aging
cardiovascular disease
morbidity
mortality
risk factors

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1161/ATVBAHA.122.317332

Cite this

Sutton, N. R., Malhotra, R., Hilaire, C. S., Aikawa, E., Blumenthal, R. S., Gackenbach, G., Goyal, P., Johnson, A., Nigwekar, S. U., Shanahan, C. M., Towler, D. A., Wolford, B. N., & Chen, Y. (2023). Molecular Mechanisms of Vascular Health: Insights From Vascular Aging and Calcification. Arteriosclerosis, Thrombosis, and Vascular Biology, 43(1), 15-29. https://doi.org/10.1161/ATVBAHA.122.317332

@article{2ed840e5610f45999addbf5e59289ced,

title = "Molecular Mechanisms of Vascular Health: Insights From Vascular Aging and Calcification",

abstract = "Cardiovascular disease is the most common cause of death worldwide, especially beyond the age of 65 years, with the vast majority of morbidity and mortality due to myocardial infarction and stroke. Vascular pathology stems from a combination of genetic risk, environmental factors, and the biologic changes associated with aging. The pathogenesis underlying the development of vascular aging, and vascular calcification with aging, in particular, is still not fully understood. Accumulating data suggests that genetic risk, likely compounded by epigenetic modifications, environmental factors, including diabetes and chronic kidney disease, and the plasticity of vascular smooth muscle cells to acquire an osteogenic phenotype are major determinants of age-associated vascular calcification. Understanding the molecular mechanisms underlying genetic and modifiable risk factors in regulating age-associated vascular pathology may inspire strategies to promote healthy vascular aging. This article summarizes current knowledge of concepts and mechanisms of age-associated vascular disease, with an emphasis on vascular calcification.",

keywords = "aging, cardiovascular disease, morbidity, mortality, risk factors",

author = "Sutton, {Nadia R.} and Rajeev Malhotra and Hilaire, {Cynthia St.} and Elena Aikawa and Blumenthal, {Roger S.} and Grace Gackenbach and Parag Goyal and Adam Johnson and Nigwekar, {Sagar U.} and Shanahan, {Catherine M.} and Towler, {Dwight A.} and Wolford, {Brooke N.} and Yabing Chen",

note = "Funding Information: N.R. Sutton is an Advisor for Philips and Abbott and receives Honoraria from Zoll, Abbott, Shockwave, and Cordis. R. Malhotra—sponsored research agreement for Amgen, Bayer; Consultant for Renovocor, Third Pole, Myokardia (now Bristol Myers Squibb). S.N. Nigwekar is a Consultant for Epizon Pharma, Laboratoris Sanifit, Inozyme Pharma and reports grant support from Hope Pharma, Laboratoris Sanifit, Inozyme Pharma. P. Goyal is a Consultant for Sensorum Health. The other authors report no conflicts. R. Malhotra was supported by the National Heart, Lung, and Blood Institute (R01HL142809), the American Heart Association (18TPA34230025), and the Wild Family Foundation. E. Aikawa is supported by research grants from the National Institutes of Health R01HL136431, R01HL141917, and R01HL147095. C.S. Hilaire holds grants from the National Institutes of Health (HL142932) and the American Heart Association (20IPA35260111). B.N. Wolford is funded by the European Union H2020 Research and Innovation programme INTERVENE (International Consortium for Integrative Genomics Prediction), grant no. 101016775. N.R. Sutton National Institute on Aging 1K76AG064426-01A1. P. Goyal is supported by American Heart Association grant 20CDA35310455, National Institute on Aging grant K76AG064428, and Loan Repayment Program award L30AG060521. S.U. Nigwekar is supported by the National Institute of Biomedical Imaging and Bioengineering (1R01EB031813-01A1) and by the National Institute of Diabetes and Digestive and Kidney Diseases (1U01DK123818-01). C.M. Shanahan is supported by grants from the British Heart Foundation (RG/17/2/32808). D.A. Towler is supported by grants from the National Institutes of Health (HL069229-21), American Diabetes Association (1-18-IBS-224), and the Pak Center for Mineral Metabolism Research. Y. Chen is supported by grants from the National Institutes of Health (HL136165, HL146103 and HL158097) as well as United States Department of Veterans Affairs Basic Sciences R&D Service (BX005800 and BX004426). Publisher Copyright: {\textcopyright} 2023 Lippincott Williams and Wilkins. All rights reserved.",

year = "2023",

month = jan,

day = "1",

doi = "10.1161/ATVBAHA.122.317332",

language = "English",

volume = "43",

pages = "15--29",

journal = "Arteriosclerosis, Thrombosis, and Vascular Biology",

issn = "1079-5642",

publisher = "Lippincott Williams and Wilkins",

number = "1",

}

Sutton, NR, Malhotra, R, Hilaire, CS, Aikawa, E, Blumenthal, RS, Gackenbach, G, Goyal, P, Johnson, A, Nigwekar, SU, Shanahan, CM, Towler, DA, Wolford, BN & Chen, Y 2023, 'Molecular Mechanisms of Vascular Health: Insights From Vascular Aging and Calcification', Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 43, no. 1, pp. 15-29. https://doi.org/10.1161/ATVBAHA.122.317332

TY - JOUR

T1 - Molecular Mechanisms of Vascular Health

T2 - Insights From Vascular Aging and Calcification

AU - Sutton, Nadia R.

AU - Malhotra, Rajeev

AU - Hilaire, Cynthia St.

AU - Aikawa, Elena

AU - Blumenthal, Roger S.

AU - Gackenbach, Grace

AU - Goyal, Parag

AU - Johnson, Adam

AU - Nigwekar, Sagar U.

AU - Shanahan, Catherine M.

AU - Towler, Dwight A.

AU - Wolford, Brooke N.

AU - Chen, Yabing

N1 - Funding Information: N.R. Sutton is an Advisor for Philips and Abbott and receives Honoraria from Zoll, Abbott, Shockwave, and Cordis. R. Malhotra—sponsored research agreement for Amgen, Bayer; Consultant for Renovocor, Third Pole, Myokardia (now Bristol Myers Squibb). S.N. Nigwekar is a Consultant for Epizon Pharma, Laboratoris Sanifit, Inozyme Pharma and reports grant support from Hope Pharma, Laboratoris Sanifit, Inozyme Pharma. P. Goyal is a Consultant for Sensorum Health. The other authors report no conflicts. R. Malhotra was supported by the National Heart, Lung, and Blood Institute (R01HL142809), the American Heart Association (18TPA34230025), and the Wild Family Foundation. E. Aikawa is supported by research grants from the National Institutes of Health R01HL136431, R01HL141917, and R01HL147095. C.S. Hilaire holds grants from the National Institutes of Health (HL142932) and the American Heart Association (20IPA35260111). B.N. Wolford is funded by the European Union H2020 Research and Innovation programme INTERVENE (International Consortium for Integrative Genomics Prediction), grant no. 101016775. N.R. Sutton National Institute on Aging 1K76AG064426-01A1. P. Goyal is supported by American Heart Association grant 20CDA35310455, National Institute on Aging grant K76AG064428, and Loan Repayment Program award L30AG060521. S.U. Nigwekar is supported by the National Institute of Biomedical Imaging and Bioengineering (1R01EB031813-01A1) and by the National Institute of Diabetes and Digestive and Kidney Diseases (1U01DK123818-01). C.M. Shanahan is supported by grants from the British Heart Foundation (RG/17/2/32808). D.A. Towler is supported by grants from the National Institutes of Health (HL069229-21), American Diabetes Association (1-18-IBS-224), and the Pak Center for Mineral Metabolism Research. Y. Chen is supported by grants from the National Institutes of Health (HL136165, HL146103 and HL158097) as well as United States Department of Veterans Affairs Basic Sciences R&D Service (BX005800 and BX004426). Publisher Copyright: © 2023 Lippincott Williams and Wilkins. All rights reserved.

PY - 2023/1/1

Y1 - 2023/1/1

N2 - Cardiovascular disease is the most common cause of death worldwide, especially beyond the age of 65 years, with the vast majority of morbidity and mortality due to myocardial infarction and stroke. Vascular pathology stems from a combination of genetic risk, environmental factors, and the biologic changes associated with aging. The pathogenesis underlying the development of vascular aging, and vascular calcification with aging, in particular, is still not fully understood. Accumulating data suggests that genetic risk, likely compounded by epigenetic modifications, environmental factors, including diabetes and chronic kidney disease, and the plasticity of vascular smooth muscle cells to acquire an osteogenic phenotype are major determinants of age-associated vascular calcification. Understanding the molecular mechanisms underlying genetic and modifiable risk factors in regulating age-associated vascular pathology may inspire strategies to promote healthy vascular aging. This article summarizes current knowledge of concepts and mechanisms of age-associated vascular disease, with an emphasis on vascular calcification.

AB - Cardiovascular disease is the most common cause of death worldwide, especially beyond the age of 65 years, with the vast majority of morbidity and mortality due to myocardial infarction and stroke. Vascular pathology stems from a combination of genetic risk, environmental factors, and the biologic changes associated with aging. The pathogenesis underlying the development of vascular aging, and vascular calcification with aging, in particular, is still not fully understood. Accumulating data suggests that genetic risk, likely compounded by epigenetic modifications, environmental factors, including diabetes and chronic kidney disease, and the plasticity of vascular smooth muscle cells to acquire an osteogenic phenotype are major determinants of age-associated vascular calcification. Understanding the molecular mechanisms underlying genetic and modifiable risk factors in regulating age-associated vascular pathology may inspire strategies to promote healthy vascular aging. This article summarizes current knowledge of concepts and mechanisms of age-associated vascular disease, with an emphasis on vascular calcification.

KW - aging

KW - cardiovascular disease

KW - morbidity

KW - mortality

KW - risk factors

UR - http://www.scopus.com/inward/record.url?scp=85144592301&partnerID=8YFLogxK

U2 - 10.1161/ATVBAHA.122.317332

DO - 10.1161/ATVBAHA.122.317332

M3 - Review article

C2 - 36412195

AN - SCOPUS:85144592301

SN - 1079-5642

VL - 43

SP - 15

EP - 29

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

IS - 1

ER -

Molecular Mechanisms of Vascular Health: Insights From Vascular Aging and Calcification

Abstract

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this