Cited by 98Cell death mechanisms and regulationCardiovascular Effects of ExerciseCardiovascular and exercise physiology

Effects of aging and exercise training on apoptosis in the heart

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Kwak, Hyo-Bum·2013·Journal of Exercise Rehabilitation

Abstract

Aging is characterized by a progressive decline in cardiac function. A critical contributor to the age-related impairment in cardiac function is the loss of cardiac myocytes through "apoptosis", or programmed cell death. Structural remodeling in the heart with advancing age includes (a) loss of cardiomyocytes, (b) reactive hypertrophy of the remaining cardiomyocytes, and (c) increased connective tissue and altered geometry. The loss of cardiomyocytes with aging occurs through apoptosis. Particularly, mitochondrial-mediated apoptotic pathway is the best characterized and believed critical in regulating apoptosis with aging, suggesting that mitochondria are very important sites of programmed cell death. It has been also reported that mitochondrial dysfunction, oxidative stress, and impaired stress response contribute to age-induced mechanical remodeling as well as apoptosis. In contrast, exercise training not only improves cardiac function, but also reduces the risk of heart disease. We recently found that aging increased mitochondrial-mediated apoptotic signaling and apoptosis in the left ventricle, while chronic exercise training was effective in diminishing mitochondrial-mediated apoptotic signaling pathways in the aging heart, as indicated by lower DNA fragmentation, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive staining, and caspase-3 cleavage, when compared with left ventricles from the age-matched sedentary group. In this review, we will provide a comprehensive update regarding the effects of aging and exercise training on apoptosis in the heart.

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  • Rodent models implicate a PCD mechanism in the aging heart involving increased Bax/Bcl-2 ratio, cytochrome c release from mitochondria and Caspase-3 activation.

    “Loss of myocytes is observed in the aging heart, and studies in rodent models implicate a PCD mechanism involving increased Bax/Bcl-2 ratio, cytochrome c release from mitochondria and Caspase-3 activation (Kwak, 2013).”

    From Programmed cell death in aging (2015) · cites this paper as Kwak, 2013

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Authors
Kwak, H.-B.
Affiliations
Inha University (KR)
Corresponding author
Kwak, Hyo-Bum
Venue
Journal of Exercise Rehabilitation
Published
2013-04-25
Volume
9
Issue
2
Pages
212-219
ISSN
  • 2288-176X (ISSN-L)
  • 2288-1778
OpenAlex
W1989446499
Cited by
98
References
83
Citations by year
2026: 2 · 2025: 2 · 2024: 6 · 2023: 7 · 2022: 9 · 2021: 13 · 2020: 16 · 2019: 9 · 2018: 7 · 2017: 7 · 2016: 10 · 2015: 5 · 2014: 5
FWCI
0.63
Type
journal article
Language
en
Open access
Locations
  • Journal of Exercise Rehabilitation (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • National Research Foundation
  • Inha University
  • National Research Foundation of Korea
  • Ministry of Education, Science and Technology
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
Keywords
cardiac aging, exercise training, apoptosis, cardiomyocyte loss, mitochondrial apoptosis, mitochondrial dysfunction, oxidative stress, cardiac remodeling, left ventricle, caspase-3, DNA fragmentation, heart failure risk

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