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Age-related vascular stiffening: causes and consequences
Open accessAbstract
Arterial stiffening occurs with age and is closely associated with the progression of cardiovascular disease. Stiffening is most often studied at the level of the whole vessel because increased stiffness of the large arteries can impose increased strain on the heart leading to heart failure. Interestingly, however, recent evidence suggests that the impact of increased vessel stiffening extends beyond the tissue scale and can also have deleterious microscale effects on cellular function. Altered extracellular matrix (ECM) architecture has been recognized as a key component of the pre-atherogenic state. Here, the underlying causes of age-related vessel stiffening are discussed, focusing on age-related crosslinking of the ECM proteins as well as through increased matrix deposition. Methods to measure vessel stiffening at both the macro- and microscale are described, spanning from the pulse wave velocity measurements performed clinically to microscale measurements performed largely in research laboratories. Additionally, recent work investigating how arterial stiffness and the changes in the ECM associated with stiffening contributed to endothelial dysfunction will be reviewed. We will highlight how changes in ECM protein composition contribute to atherosclerosis in the vessel wall. Lastly, we will discuss very recent work that demonstrates endothelial cells (ECs) are mechano-sensitive to arterial stiffening, where changes in stiffness can directly impact EC health. Overall, recent studies suggest that stiffening is an important clinical target not only because of potential deleterious effects on the heart but also because it promotes cellular level dysfunction in the vessel wall, contributing to a pathological atherosclerotic state.
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“EC dysfunction has been shown to strongly affect arterial stiffness via cellular adhesion molecules (CAMs), matrix metalloproteinases (MMPs) and collagen molecules (COLs)67–71.”
From An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging (2021) · cites this paper as [68]
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“Thus, an increase in Pxdn might contribute to the arterial stiffening that is observed in atherosclerosis (72).”
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Freidoonimehr, N., Chin, R. C., Zander, A. C., & Arjomandi, M. (2020) · Physics of Fluids · doi:10.1063/1.5139701 · Cited by 44
Zhu, W., Kim, B. C., Wang, M., Huang, J., Isak, A., Bexiga, N. M., Monticone, R. E., Ha, T., Lakatta, E. G., & An, S. S. (2018) · Scientific Reports · doi:10.1038/s41598-018-20763-w · Cited by 45
Abdelkarim, D., Zhao, Y., Turner, M. P., Sivakolundu, D. K., Lu, H., & Bart Rypma, A. (2019) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2019.09.005 · Cited by 47
Feresin, R. G., Johnson, S. A., Pourafshar, S., Campbell, J. C., Jaime, S. J., Navaei, N., Elam, M. L., Akhavan, N. S., Alvarez‐Alvarado, S., Tenenbaum, G., et al. (2017) · Food & Function · doi:10.1039/c7fo01183k · Cited by 44
Central systolic pressure and a nonessential amino acid metabolomics profile
Mels, C. M. C., Delles, C., Louw, R., & Schutte, A. E. (2019) · Journal of Hypertension · doi:10.1097/hjh.0000000000002040 · Cited by 43
“This implies an important requisite for glycine bioavailability to support healthy collagen turnover [44] and consequently arterial elasticity [45].”
BackgroundCostameres, dense plaques and podosomes: the cell matrix adhesions in cardiovascular mechanosensing
Sit, B. H. M., Gutmann, D., & Iskratsch, T. (2019) · Journal of Muscle Research and Cell Motility · doi:10.1007/s10974-019-09529-7 · Cited by 40
Effect of heart rate on the hemodynamics in healthy and stenosed carotid arteries
Khan, P. M., Sharma, S. D., Chakraborty, S. K., & Roy, S. (2023) · Physics of Fluids · doi:10.1063/5.0153323 · Cited by 40
The Potential Role of Creatine in Vascular Health
Clarke, H. E., Hickner, R. C., & Ormsbee, M. J. (2021) · Nutrients · doi:10.3390/nu13030857 · Cited by 44
Kleefeldt, F., Bömmel, H. M., Broede, B., Thomsen, M., Pfeiffer, V., Wörsdörfer, P., Karnati, S., Wagner, N., Rueckschloss, U., & Ergün, S. (2019) · Aging Cell · doi:10.1111/acel.13025 · Cited by 39
Transitional turbulent flow in a stenosed coronary artery with a physiological pulsatile flow
Freidoonimehr, N., Arjomandi, M., Sedaghatizadeh, N., Chin, R. C., & Zander, A. C. (2020) · International Journal for Numerical Methods in Biomedical Engineering · doi:10.1002/cnm.3347 · Cited by 39
3D Printing Applied to Tissue Engineered Vascular Grafts
Wenger, R., & Giraud, M. (2018) · Applied Sciences · doi:10.3390/app8122631 · Cited by 38
“5 MPa and varies with age and health status [7,8].”
BackgroundMechanical damage characterization in human femoropopliteal arteries of different ages
Anttila, E. D., Balzani, D., Desyatova, A. S., Deegan, P. T., MacTaggart, J., & Kamenskiy, A. V. (2019) · Acta Biomaterialia · doi:10.1016/j.actbio.2019.03.053 · Cited by 38
Park, W., Park, H., Lim, K., & Park, J. (2017) · Physical Activity and Nutrition · doi:10.20463/jenb.2017.0041 · Cited by 36
“In addition, arterial stiffness is associated with low physical activity levels in Japanese community-dwelling older adults [15].”
BackgroundVascular smooth muscle cell contractile function and mechanotransduction
Ahmed, S., & Warren, D. T. (2018) · Vessel Plus · doi:10.20517/2574-1209.2018.51 · Cited by 37
“However, ECM deformation was used to assess the vasoconstrictor response and given that aged arteries are stiffer than their younger counterparts, VSMC actomyosin activity may remain intact([97]).”
MethodFibrillar Collagen: A Review of the Mechanical Modeling of Strain-Mediated Enzymatic Turnover
Topol, H., Demirkoparan, H., & Pence, T. J. (2021) · Applied Mechanics Reviews · doi:10.1115/1.4052752 · Cited by 35
Fibroblasts in Pulmonary Hypertension: Roles and Molecular Mechanisms
Zhang, H., Li, M., Hu, C., & Stenmark, K. R. (2024) · Cells · doi:10.3390/cells13110914 · Cited by 40
“…vascular remodeling is characterized by the emergence of a distinct adventitial fibroblast population that exhibits a constitutively activated, or “imprinted”, proinflammatory phenotype capable of inducing the recruitment, retention, and proinflammatory activation of monocytes and macrophages [8].”
BackgroundMechanical heterogeneities in the subendothelial matrix develop with age and decrease with exercise
Kohn, J. C., Chen, A., Cheng, S. W., Kowal, D. R., King, M. R., & Reinhart‐King, C. A. (2016) · Journal of Biomechanics · doi:10.1016/j.jbiomech.2016.03.016 · Cited by 34
“Kohn et al. / Journal of Biomechanics 49 (2016) 1447–1453 1448”
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“This enabled us to focus exclusively on the mechanical properties of the tissue fibers and how they change with age, the latter being known to principally affect the fibers (Kohn et al., 2015; Panwar et al., 2015).”
BackgroundVascular Ageing and Aerobic Exercise
Kozàkovà, M., & Palombo, C. (2021) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph182010666 · Cited by 34
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Increased Substrate Stiffness Elicits a Myofibroblastic Phenotype in Human Lamina Cribrosa Cells
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Maleckis, K., Kamenskiy, A. V., Lichter, E. Z., Oberley‐Deegan, R. E., Dzenis, Y. A., & MacTaggart, J. (2021) · Acta Biomaterialia · doi:10.1016/j.actbio.2021.01.047 · Cited by 32
“The deleterious effects of aging and other risk factors result in structural changes in the arterial wall, leading to increased stiffness and the development of vascular disease [36-38].”
BackgroundNuclear softening mediated by Sun2 suppression delays mechanical stress-induced cellular senescence
Yue, X., Cui, J., Sun, Z., Liu, L., Li, Y., Shao, L., Feng, Q., Wang, Z., Hambright, W. S., Cui, Y., et al. (2023) · Cell Death Discovery · doi:10.1038/s41420-023-01467-1 · Cited by 32
Comparative mechanics of diverse mammalian carotid arteries
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Advances in mechanical biomarkers
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“replaced in the human body and its loss, through genetic or acquired factors, conducts to several diseases that have been proven to change the mechanical properties of the arteries.(217) Genetic diseases in elas-”
Backgroundvon Kleeck, R. A., Roberts, E., Castagnino, P. A., Bruun, K., Brankovic, S. A., Hawthorne, E. A., Xu, T., Tobias, J. W., & Assoian, R. K. (2021) · Life Science Alliance · doi:10.26508/lsa.202000997 · Cited by 28
“Elastin allows for recoil at lower load and dampens cyclic loading from the beating heart, whereas fi brillar collagens contribute to the strain-stiffening property of arteries at high load (Kohn et al, 2015).”
Aortic Pulse Wave Velocity Evaluated by 4D Flow MRI Across the Adult Lifespan
Jarvis, K., Scott, M., Soulat, G., Elbaz, M. S. M., Barker, A. J., Carr, J. C., Markl, M., & Ragin, A. B. (2022) · Journal of Magnetic Resonance Imaging · doi:10.1002/jmri.28045 · Cited by 30
“Aortic PWV correlated with age which is likely due to changes in elastin fibers during the aging process.(32) Our correlation results for PWV with age agree well with a study also using cross-correlation in 57 healthy individuals,(16) demonstrating agreement between institutions using different scanner platforms and d…”
ResultMaster, E. L., Paul, A., Lazarko, D., Aguilar, V. M., Ahn, S. J., Lee, J. C., Minshall, R. D., & Levitan, I. (2022) · Scientific Reports · doi:10.1038/s41598-022-20713-7 · Cited by 30
Endothelial Senescence and Its Impact on Angiogenesis in Alzheimer’s Disease
Georgieva, I., Tchekalarova, J. D., Iliev, D. B., & Tzoneva, R. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241411344 · Cited by 29
“Meanwhile, collagen secretion increases, causing the stiffening of ECM in an NAD+-dependent manner [69].”
BackgroundKerch, G. (2018) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2018.06.187 · Cited by 32
Biomimetic Vasculatures by 3D‐Printed Porous Molds
Ching, T., Vasudevan, J., Chang, S., Tan, H. Y., Ranganath, A. S., Lim, C. T., Fernandez, J. G., Ng, J. J., Toh, Y., & Hashimoto, M. (2022) · Small · doi:10.1002/smll.202203426 · Cited by 29
Babar, F., Cheema, A. M., Ahmad, Z., Sarfraz, A., Sarfraz, Z., Ashraff, H., Tayyab, H., Bajwa, A. M., Ali, H., Sarfraz, M., et al. (2023) · Current Cardiology Reports · doi:10.1007/s11886-023-01898-3 · Cited by 31
Metadata
- Authors
- Kohn, J. C., Lampi, M. C., & Reinhart-King, C. A.
- Affiliations
- Cornell University (US)
- Venue
- Frontiers in Genetics
- Publisher
- Frontiers Media SA
- Published
- 2015-03-30
- Volume
- 06
- Pages
- 112-112
- ISSN
- 1664-8021 (ISSN-L)
- PMC
- PMC4396535
- OpenAlex
- W2048903244
- Cited by
- 440
- References
- 229
- Citations by year
- 2026: 45 · 2025: 36 · 2024: 58 · 2023: 60 · 2022: 46 · 2021: 51 · 2020: 36 · 2019: 29 · 2018: 40 · 2017: 26 · 2016: 11 · 2015: 1
- FWCI
- 4.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Genetics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Science Foundation (1435755, 2013165170, 2013155462)
- National Heart, Lung, and Blood Institute (R21HL097296, HL097296)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Physical Sciences › Engineering › Biomedical Engineering › Elasticity and Material Modeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Keywords
- arterial stiffening, aging, extracellular matrix, matrix deposition, pulse wave velocity, endothelial dysfunction, atherosclerosis, cardiovascular disease, heart failure
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