ArticleStem cell research & therapy2025
Miro1 protects against brain injury after CPR in rats by enhancing the effect of BMSCs on mitochondrial homeostasis.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Proton Radiation-Induced Cognitive Impairment via Disruption of Hippocampal Neuronal Mitophagic Homeostasis.Biomolecules · 2026Article
- Mitochondrial transfer: a novel paradigm for wound healing.Burns & trauma · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
backgroundMitochondrial dyshomeostasis plays an important role in neuronal damage after cerebral ischemia-reperfusion, and Miro1 is a core protein that regulates mitochondrial homeostasis. In this study, we aimed to investigate the neuroprotective effects of bone marrow-derived mesenchymal stem cells (BMSCs) via mitochondrial homeostasis in rats after cardiac arrest (CA), and to clarify the role that the protein Miro1 plays in this protective efficacy.
methodsThe study compared the effects of BMSCs in which Miro1 was overexpressed BMSCs (BMSCs-miro
resultsImmunofluorescence staining revealed the presence of mitochondria from MitoTracker-labeled BMSCs in rat hippocampal neurons post-CPR. Additionally, the fluorescence intensity of TOMM20 was notably increased following the transplantation of BMSCs. Through immunoblotting experiments, we identified that BMSCs amplified the post-CPR protein expression of LC3, p62, PINK1 and parkin in hippocampal neurons. The number of autophagosomes significantly increased in hippocampal neurons following BMSC transplantation, as observed through transmission electron microscopy. Flow cytometry, Hematoxylin and Eosin (HE) staining, and NDS scoring indicated that BMSCs effectively reduced reactive oxygen species accumulation in hippocampal neurons and mitochondria after CPR. Furthermore, they restored mitochondrial membrane potential and ATP levels in the hippocampus while decreasing apoptosis, ultimately contributing to the restoration of neurological function. Additionally, unlike BMSCs-miro
conclusionsThese analyses revealed that BMSC transplantation has a dual protective effect by facilitating healthy mitochondrial transfer and promoting the autophagic degradation of damaged mitochondria, effectively enhancing hippocampal neuronal mitochondrial function following CA while reducing neuronal apoptosis, restoring neuronal function, and alleviating neuropathological damage. Moreover, Miro1 can enhance the efficiency of mitochondrial transfer and promote BMSC-mediated mitophagy induction, thereby optimizing the therapeutic effect of BMSCs.
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