ArticleIranian journal of basic medical sciences2023
Chronic stress-induced apoptosis is mitigated by young mitochondria transplantation in the prefrontal cortex of aged rats.
Article in Iranian journal of basic medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Mitochondrial transplantation for delirium superimposed on dementia: from pathogenic mechanisms to clinical translation challenges.Frontiers in aging neuroscience · 2026Review
- Therapeutic transplantation of mitochondria and Extracellular Vesicles: Mechanistic insights into mitochondria bioenergetics, redox signaling, and organelle dynamics in preclinical models.Free radical biology & medicine · 2025Review
- Non-pharmacological therapeutic paradigms in stress-induced depression: from novel therapeutic perspective with focus on cell-based strategies.Acta neuropsychiatrica · 2025Review
- Recent advances in mitochondrial transplantation to treat disease.Biomaterials translational · 2025Review
- Mitochondrial transplantation and transfer: The promising method for diseases.Turkish journal of biology = Turk biyoloji dergisi · 2023Review
- Comparative analysis of mitochondrial and mesenchymal stem cell transplantation for angiogenesis and muscle regeneration.Cell transplantationArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Objectives: Apoptosis is common and often comorbid with aging and stress-related mood disorders. Evidence suggests that fresh mitochondria could reverse age-related dysfunctions in organs, especially in the brain. Therefore, this study investigated the effect of young mitochondria administration on the apoptosis process in the prefrontal cortex (PFC) of aged rats exposed to chronic stress. Materials and Methods: Aged (22 months old) male rats were randomly assigned into four groups: aged control (AC), aged rats treated with young mitochondria (A+M), aged rats subjected to chronic stress for four weeks (A+St), and aged rats subjected to chronic stress and treated with young mitochondria (A+St+M). A+M and A+St+M groups received a single ICV injection (10 μl) of fresh mitochondria isolated from the brain of young rats for five minutes (2 µl/min). Finally, the levels of Malondialdehyde (MDA), Cytochrome c (Cyt c), Bax, Bcl-2, and Caspase-3 expression were investigated in the PFC. Results: Young mitochondria administration reduced neuronal apoptosis in the PFC, associated with down-regulation of MDA, Bax, and Caspase-3 and up-regulation of Bcl-2. Moreover, fresh mitochondria partially improved the chronic stress-induced mitochondrial dysfunction in aged rats, as indicated by reduced cytochrome c (Cyt c) release from the mitochondria. Conclusion: These results suggest mitotherapy could reverse cell viability and mitochondrial dysfunction-induced apoptosis in the PFC tissue of aged rats subjected to stressful stimuli.
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