The aging heart
Abstract
As the elderly segment of the world population increases, it is critical to understand the changes in cardiac structure and function during the normal aging process. In this review, we outline the key molecular pathways and cellular processes that underlie the phenotypic changes in the heart and vasculature that accompany aging. Reduced autophagy, increased mitochondrial oxidative stress, telomere attrition, altered signaling in insulin-like growth factor, growth differentiation factor 11, and 5′- AMP-activated protein kinase pathways are among the key molecular mechanisms underlying cardiac aging. Aging promotes structural and functional changes in the atria, ventricles, valves, myocardium, pericardium, the cardiac conduction system, and the vasculature. We highlight the factors known to accelerate and attenuate the intrinsic aging of the heart and vessels in addition to potential preventive and therapeutic avenues. A greater understanding of the processes involved in cardiac aging may facilitate our ability to mitigate the escalating burden of CVD in older individuals and promote healthy cardiac aging.
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During aging, dysfunction and decline of vascular smooth muscle cells impair the structural integrity of the aorta, leading to transthoracic aortic aneurysms.
“However, during the aging process, the dysfunction and decline of VSMCs have a detrimental impact on the structural integrity of the aorta, ultimately leading to the development of transthoracic aortic aneurysms.142”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [142]
The decline in AMPK and GDF11 expression associated with aging is likely a contributing factor to the heightened cardiac fibrosis observed during aging.
“The cardioprotective effects of AMPK and GDF11 on cardiomyocytes have been extensively documented, and the decline in AMPK and GDF11 expression associated with aging is likely a contributing factor to the heightened cardiac fibrosis observed during the aging process.142”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [142]
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References 158 · Cited by 148
- Authors
- Obas, V., & Vasan, R. S.
- Affiliations
- Boston University (US)
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2018-07-09
- Volume
- 132
- Issue
- 13
- Pages
- 1367-1382
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- OpenAlex
- W2869995163
- Cited by
- 148
- References
- 158
- Citations by year
- 2026: 14 · 2025: 32 · 2024: 20 · 2023: 23 · 2022: 14 · 2021: 23 · 2020: 14 · 2019: 7 · 2018: 1
- FWCI
- 2.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hl080124-05)
- National Heart, Lung, and Blood Institute (R01-HL080124, HHSN268201500001I, R01HL126136)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- cardiac aging, heart structure and function, autophagy, mitochondrial oxidative stress, telomere shortening, insulin-like growth factor signaling, GDF11, AMPK, cardiac conduction system, cardiac vasculature, atrium, ventricles, heart valves, cardiovascular disease in older adults, healthy aging
- MeSH terms
- Aging, Autophagy, Heart, Humans, Signal Transduction, Oxidative Stress, Insulin-Like Growth Factor Binding Protein 1, Ventricular Remodeling, Telomere Shortening
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