ArticleLife (Basel, Switzerland)2020
Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts.
Article in Life (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Resveratrol attenuates aging-induced mitochondrial dysfunction and mitochondria-mediated apoptosis in the rat heart.Nutrition research and practice · 2025Article
- Dysfunctional mitochondria elicit bioenergetic decline in the aged heart.The journal of cardiovascular aging · 2024Article
- Unlocking the dark matter: noncoding RNAs and RNA modifications in cardiac aging.American journal of physiology. Heart and circulatory physiology · 2024Review
- Article
- Effect of vitamin D on cardiac hypertrophy in D-galactose-induced aging model through cardiac mitophagy.Molecular biology reports · 2023Article
- Article
- Excess heme upregulates heme oxygenase 1 and promotes cardiac ferroptosis in mice with sickle cell disease.Blood · 2022Article
- Impaired Mitochondrial Bioenergetics under Pathological Conditions.Life (Basel, Switzerland) · 2022Article
- Keeping the beat against time: Mitochondrial fitness in the aging heart.Frontiers in aging · 2022Review
- Melatonin/Nrf2/NLRP3 Connection in Mouse Heart Mitochondria during Aging.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Aging represents a major risk for developing cardiac disease, including heart failure. The gradual deterioration of cell quality control with aging leads to cell death, a phenomenon associated with mitochondrial dysfunction in the heart. Apoptosis is an important quality control process and a necessary phenomenon for maintaining homeostasis and normal function of the heart. However, the mechanism of mitochondria-mediated apoptosis in aged hearts remains poorly understood. Here, we used male Fischer 344 rats of various ages, representing very young (1 month), young (4 months), middle-aged (12 months), and old (20 months) rats, to determine whether mitochondria-mediated apoptotic signals and apoptosis in the left ventricle of the heart are altered notably with aging. As the rats aged, the extramyocyte space and myocyte cross-sectional area in their left ventricle muscle increased, while the number of myocytes decreased. Additionally, mitochondrion-mediated apoptotic signals and apoptosis increased remarkably during aging. Therefore, our results demonstrate that aging promotes remarkable morphological changes and increases the degree of mitochondrion-mediated apoptosis in the left ventricle of rat hearts.
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Registered trials
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