ArticleNeurochemical research2021
Remote Ischemic Postconditioning Inhibited Mitophagy to Achieve Neuroprotective Effects in the Rat Model of Cardiac Arrest.
Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- EV-Encapsulated Mitochondrial miRNAs: Enhancing Cardiomyocyte Bioenergetics.International journal of molecular sciences · 2026Review
- Hemodynamics of active abdominal compression decompression CPR in a rat model of multiple rib fractures with asphyxial cardiac arrest.Scientific reports · 2025Article
- Translational approach to assess brain injury after cardiac arrest in preclinical models: a narrative review.Intensive care medicine experimental · 2025Review
- Review
- Secretory Factors from Calcium-Sensing Receptor-Activated SW872 Pre-Adipocytes Induce Cellular Senescence and A Mitochondrial Fragmentation-Mediated Inflammatory Response in HepG2 Cells.International journal of molecular sciences · 2023Article
- Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury.Life (Basel, Switzerland) · 2021Review
- Effects of Mdivi-1 on Neural Mitochondrial Dysfunction and Mitochondria-Mediated Apoptosis in Ischemia-Reperfusion Injury After Stroke: A Systematic Review of Preclinical Studies.Frontiers in molecular neuroscience · 2021Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Remote ischemic postconditioning (RI-postC) is an effective measure to improve nerve function after cardiac arrest. However, the brain protective mechanism of RI-postC has not been fully elucidated, and whether it is related to mitophagy is unclear. In this study, we used the rat model of cardiac arrest to study the effect of RI-postC on mitophagy and explore its possible signaling pathways. Rats were randomly divided into Sham group, CA/CPR group, Mdivi-1 group and RI-postC group. The animal model of cardiac arrest was established by asphyxia. RI-postC was performed by clamping and loosening the left femoral artery. Mdivi-1 was treated with a single intravenous injection. Levels of TOMM20, TIM23, Mfn1, PINK1 and parkin were detected by western blots. Mitochondrial membrane potential was measured by flow cytometry. Real-time PCR was used to detect relative mitochondrial DNA levels. The apoptosis of hippocampal neurons was detected by flow and TUNEL. In addition, Histopathological tests were performed. The results showed that RI-postC was similar to the mitophagy inhibitor Mdivi-1, which could inhibit the decrease of mitophagy-related protein level, improve mitochondrial membrane potential and up-regulate the ratio of mt-Atp6/Rpl13 after cardiopulmonary resuscitation (CPR). Furthermore, RI-postC could also reduce the rate of hippocampal nerve apoptosis and the damage of hippocampal neurons after CPR. Moreover, RI-postC and Mdivi-1 could reduce the protein levels of PINK1 and parkin in mitochondria after CPR, while increasing PINK1 levels in the cytoplasm. These findings suggested that RI-postC could inhibit the overactivation mitophagy through the PINK1/parkin signaling pathway, thus providing neuroprotective effects.
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