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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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Cellular senescence in age-related cardiovascular disease: past and future
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“For example, vascular endothelial cell dysfunction has been shown to affect arteriosclerosis through cell adhesion molecules (CAMs), MMPs, and collagen molecules (COLs) (Kohn et al., 2015; Kuzuya et al., 2001; Zieman et al., 2005).”
Brutto, V. J. D., Khasiyev, F., Liu, M., Spagnolo‐Allende, A., Qiao, Y., Arias, J. D. M., Guzman, V. A., Igwe, K. C., Sanchez, D. L., Andrews, H., et al. (2023) · The Neuroradiology Journal · doi:10.1177/19714009231224429 · Cited by 5
“35 Also, age-related buildup of fatty plaques within arteries (i.e., atherosclerosis) can cause arterial narrowing and stenosis, which can result in compensatory larger diameters in unaffected arterial segments that provide collateral fl ow.”
BackgroundMorgan, A. G., Thrippleton, M. J., Stringer, M. S., Chappell, F. M., Hernández, M. D. C. V., Wiseman, S. J., Ballerini, L., Brown, R., Cheng, Y., Liu, X., et al. (2025) · Stroke · doi:10.1161/strokeaha.124.049103 · Cited by 5
Karunakaran, K. D., Ji, K., Chen, D. Y., Chiaravalloti, N. D., Niu, H., Alvarez, T. L., & Biswal, B. B. (2021) · Brain Topography · doi:10.1007/s10548-021-00818-4 · Cited by 7
Cell contractility and focal adhesion kinase control circumferential arterial stiffness
Roberts, E., Xu, T., & Assoian, R. K. (2022) · Vascular Biology · doi:10.1530/vb-22-0013 · Cited by 5
“Arterial stiffening with aging and vascular disease has often been viewed as a consequence of ECM remodeling (typically, increased abundance of fibrillar collagens and/ 4 :1 or degradation of elastin (2, 3)).”
Sapkota, A., Halder, S. K., & Milner, R. (2023) · Microvascular Research · doi:10.1016/j.mvr.2023.104625 · Cited by 5
Azizi, L., Otani, Y., Mykuliak, V. V., Goult, B. T., Hytönen, V. P., & Turkki, P. (2024) · Human Molecular Genetics · doi:10.1093/hmg/ddae120 · Cited by 5
Identification of potentially causative drugs associated with hypotension: A scoping review
Sari, N., Jaehde, U., & Wermund, A. M. (2024) · Archiv der Pharmazie · doi:10.1002/ardp.202400564 · Cited by 5
Evani, S. J., Dallo, S. F., & Ramasubramanian, A. K. (2016) · Frontiers in Microbiology · doi:10.3389/fmicb.2016.01287 · Cited by 5
“Atherosclerosis is an ongoing inflammatory response (Libby et al., 2002).”
Emmert, K., Zöller, D., Preti, M. G., Ville, D. V. D., Giannakopoulos, P., & Haller, S. (2016) · PLoS ONE · doi:10.1371/journal.pone.0161121 · Cited by 5
Concannon, J., Hynes, N., McMullen, M., Smyth, E., Moerman, K. M., McHugh, P. E., Sultan, S., Karmonik, C., & McGarry, P. (2020) · Journal of Biomechanical Engineering · doi:10.1115/1.4048649 · Cited by 5
Park, W., Park, H., Lim, K., & Park, J. (2017) · Physical Activity and Nutrition · doi:10.20463/jenb.2017.16 · Cited by 5
Wearable Ambulatory Accelerometer System for Estimating Arterial Stiffness: A Pilot Study
Girish, V. V., Kiran, R. V., Nabeel, P. M., Sivaprakasam, M., & Joseph, J. (2023) · Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) · doi:10.1109/embc40787.2023.10340560 · Cited by 5
“Arterial stiffness or loss of elasticity indicates the cumulative damage incurred by the vessels, involving both arteriosclerosis and atherosclerosis [3].”
BackgroundHigh-Fat, High-Sugar Diet-Induced Subendothelial Matrix Stiffening is Mitigated by Exercise
Kohn, J. C., Azar, J., Seta, F., & Reinhart‐King, C. A. (2017) · Cardiovascular Engineering and Technology · doi:10.1007/s13239-017-0335-9 · Cited by 5
“In addition, after consumption of a Western diet, implementation of an exercise regimen has been shown to decrease [7] or to cause no effect [8] on macro-scale arterial stiffness, however less is known about the effects of exercise on the specific mechanics of the arterial intima [5].”
Self-citationThoracic aorta thickness and histological changes with aging: an experimental rat model.
Gequelim, G. C., Veronez, D. A. D. L., Marques, G. L., Tabushi, C. H., & Bueno, R. R. L. (2019) · Europe PMC (PubMed Central) · doi:10.11909/j.issn.1671-5411.2019.07.001 · Cited by 5
Kuzan, A., Michel, O., & Gamian, A. (2017) · Folia Biologica · doi:10.14712/fb2017063030105 · Cited by 5
“Kohn et al. (2015) postulated that the increase in rigidity of the ECM enhances proliferation and migration induced by platelet-derived growth factor (PDGF) released by endothelial cells and macrophages in the process of atherogenesis.”
BackgroundResultReview of Blood Pressure Control in Vulnerable Older Adults: The Role of Frailty and Sarcopenia
Sarnaik, K. S., & Mirzai, S. (2025) · Journal of Vascular Diseases · doi:10.3390/jvd4020018 · Cited by 7
“As age advances, arteries progressively stiffen due to multiple factors primarily affecting the intimal and medial layers, including reduced and damaged elastin, increased collagen deposition, and calcification [38–40].”
Bishay, A. E., Jain, H., Chanbour, H., Chen, J. W., Metcalf, T., Lyons, A. T., Abtahi, A. M., Younus, I., Stephens, B. F., & Zuckerman, S. L. (2025) · Asian Spine Journal · doi:10.31616/asj.2025.0154 · Cited by 4
“The aging population is prone to developing co-morbidities, which, along with decreased elasticity of blood vessels, affect hemostasis in older patients [27].”
Obino, G., Sensini, A., ten Brink, T., Nieddu, G., Bodet, T., Deiana, G. A., van Griensven, M., Formato, M., Lepedda, A. J., & Moroni, L. (2026) · Advanced Healthcare Materials · doi:10.1002/adhm.202505314 · Cited by 4
“Their prevalence continues to rise due to lifestyle factors and an aging global population [4, 5].”
Raval, A., Parikh, J. K., & Desai, M. A. (2023) · Journal of the mechanical behavior of biomedical materials/Journal of mechanical behavior of biomedical materials · doi:10.1016/j.jmbbm.2023.105853 · Cited by 4
Wang, Y., Wang, H., Zhou, J., Wang, J., Wu, H., & Wu, J. (2023) · International Journal of Nursing Sciences · doi:10.1016/j.ijnss.2023.06.008 · Cited by 5
“It has been established that atherosclerotic vascular impairment develops with age, and several risk factors for cardiovascular disease (CVD), including hyperlipidemia, diabetes, and smoking, can also accelerate this progression [11,12].”
BackgroundLlop, D., Feliu, A., Ibarretxe, D., Escribano, J., Plana, N., Rodríguez-Borjabad, C., Masana, L., & Vallvé, J.-C. (2023) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2023.06.012 · Cited by 4
An Update on Mitral Valve Aging
Opris, C. E., Suciu, H., Opriş, C. I., & Gurzu, S. (2024) · Life · doi:10.3390/life14080950 · Cited by 4
“In aged valves there is a change in the type I and type III collagen ratio that affects the valves’ thickness and stiffness, with the same effect produced by the increase in the local synthesis of proteoglycans and glycosaminoglycans [38].”
BackgroundYu, A. R., Hasjim, B. J., Yu, L. E., Gabriel, C., Anshus, A., Lee, J. B., Louthan, M., Kim, E. C., Lee, K., Tse, C., et al. (2017) · World Journal of Emergency Medicine · doi:10.5847/wjem.j.1920-8642.2017.03.003 · Cited by 4
Carreon, C. K., Sanders, S. P., Ferraro, A. M., Gauvreau, K., Nathan, M., Toba, S., Newburger, J. W., Beroukhim, R. S., & Quiñonez, L. G. (2023) · JTCVS Open · doi:10.1016/j.xjon.2023.07.020 · Cited by 4
Marumo, M., Ebara, S., Nishibe, I., Soneda, J., & Wakabayashi, I. (2018) · International journal of gerontology · doi:10.1016/j.ijge.2017.05.004 · Cited by 4
Bastounis, E. E., Ortega, F. E., Serrano, R., & Theriot, J. A. (2018) · Journal of Visualized Experiments · doi:10.3791/57361-v · Cited by 4
Indexing cerebrovascular health using near-infrared spectroscopy
Afkhami, R. G., Walker, F. R., Ramadan, S. A., Wong, R. H. X., & Johnson, S. J. (2021) · Scientific Reports · doi:10.1038/s41598-021-94348-5 · Cited by 4
Mack, C. P. (2024) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.124.321334 · Cited by 4
Neurobiological Mechanisms of Cognitive Decline Correlated with Brain Aging
Zhang, X., An, H., Chen, Y., & Shu, N. (2023) · Advances in experimental medicine and biology · doi:10.1007/978-981-99-1627-6_10 · Cited by 4
Cerebrovascular remodeling in aging and neurodegenerative disease progression
Halvorsen, S. C., Gkousioudi, A., Nicks, R., Alvarez, V. E., Bigio, I. J., Zaia, J., Stein, T. D., & Zhang, Y. (2025) · Frontiers in Bioengineering and Biotechnology · doi:10.3389/fbioe.2025.1597917 · Cited by 3
“Cardiovascular aortic stiffening with age is well documented and is closely associated with the progression of many diseases (McEniery et al., 2007; Kohn et al., 2015).”
The unfolded protein response in progeria arteries originates from non-endothelial cell types
Silva, R. A., Sarigol, F., Karagöz, G. E., Osmanagic‐Myers, S., & Foisner, R. (2025) · Life Science Alliance · doi:10.26508/lsa.202503485 · Cited by 4
“CVD progression has been linked to arterial stiffening, which occurs in both the physiological (Kohn et al, 2015) and premature HGPS aging (Olive et al, 2010).”
Analysis of the Second Derivative of the PPG Signal as Indicator of Vascular Aging
Diana, G., Scardulla, F., Pasta, S., & D’Acquisto, L. (2025) · International Electronic Conference on Sensors and Applications (ECSA) · doi:10.3390/ecsa-12-26557 · Cited by 3
“Since there was no direct measure of arterial stiffness for each individual, the d/a ratio was related to the age of the participants, considering that increasing age is generally associated with an increase in arterial stiffness [20].”
Hou, Y. X., Hu, X., Cheng, Q., Xie, W., Ma, L., Zhang, L., Han, X., Tan, Y., Lin, Y., Fang, C., et al. (2026) · ACS Nano · doi:10.1021/acsnano.5c19367 · Cited by 3
Cho, S., Lee, J., Park, S. C., Park, H. S., Lee, D. H., & Lee, J. (2023) · Review of Scientific Instruments · doi:10.1063/5.0087584 · Cited by 3
Gowda, P. C., Weinstein, R. M., Bhargava, A., Senarathna, J., Stewart, R. Q., Ekbote, P. V., Singh, M., Guan, E., Banghar, S., Pathak, A. P., et al. (2024) · Cardiovascular Engineering and Technology · doi:10.1007/s13239-024-00749-8 · Cited by 3
“Vero-Clear, the print material used, has a modulus of elasticity of 2000–3000 MPa, whereas arterial moduli of elasticity have been reported between 0.1 and 3 kPa [19, 20].”
InfluentialChakraborty, B., Sain, S., Mandal, D. K., Manna, N. K., Pati, S., & Santra, S. (2025) · The European Physical Journal Special Topics · doi:10.1140/epjs/s11734-025-01885-5 · Cited by 3
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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