ArticlePeerJ2016
Sevoflurane postconditioning attenuates cardiomyocyte hypoxia/reoxygenation injury via restoring mitochondrial morphology.
Article in PeerJ, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Interaction Between Rumen Microbiota and Epithelial Mitochondrial Dynamics in Tibetan Sheep: Elucidating the Mechanism of Rumen Epithelial Energy Metabolism.Biotech (Basel (Switzerland)) · 2025Article
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Sevoflurane postconditioning attenuates cardiomyocytes hypoxia/reoxygenation injury via PI3K/AKT pathway mediated HIF-1α to regulate the mitochondrial dynamic balance.BMC cardiovascular disorders · 2024Article
- Dexmedetomidine Pre-Treatment of Neonatal Rats Prevents Sevoflurane-Induced Deficits in Learning and Memory in the Adult Animals.Biomedicines · 2023Article
- Salvianolic acids and its potential for cardio-protection against myocardial ischemic reperfusion injury in diabetes.Frontiers in endocrinology · 2023Review
- Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review).Experimental and therapeutic medicine · 2022Review
- Targeted Mitochondrial Drugs for Treatment of Ischemia-Reperfusion Injury.Current drug targets · 2022Review
- Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury.Life (Basel, Switzerland) · 2021Review
- Therapeutic potential and recent advances on targeting mitochondrial dynamics in cardiac hypertrophy: A concise review.Molecular therapy. Nucleic acids · 2021Review
- Sevoflurane Postconditioning Reduces Hypoxia/Reoxygenation Injury in Cardiomyocytes via Upregulation of Heat Shock Protein 70.Journal of microbiology and biotechnology · 2021Article
- Sevoflurane exerts improved protective effects than propofol on hypoxia-reoxygenation injury by regulating the microRNA-221-5p/ADAM8 axis in cardiomyocytes.Experimental and therapeutic medicine · 2021Article
- Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling.Oxidative medicine and cellular longevity · 2021Article
- Mitochondrial quality control mechanisms as molecular targets in cardiac ischemiaActa pharmaceutica Sinica. B · 2020Review
- Sevoflurane Postconditioning Reduces Hypoxia-Reoxygenation Injury in H9C2 Embryonic Rat Cardiomyocytes and Targets the STRADA Gene by Upregulating microRNA-107.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
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- Activation of protein kinase C-α/heme oxygenase-1 signaling pathway improves mitochondrial dynamics in lipopolysaccharide-activated NR8383 cells.Experimental and therapeutic medicine · 2018Article
- Effect of sevoflurane on the ATPase activity of hippocampal neurons in a rat model of cerebral ischemia-reperfusion injury via the cAMP-PKA signaling pathway.The Kaohsiung journal of medical sciences · 2018Article
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Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnesthetic postconditioning is a cellular protective approach whereby exposure to a volatile anesthetic renders a tissue more resistant to subsequent ischemic/reperfusion event. Sevoflurane postconditioning (SPostC) has been shown to exert cardioprotection against ischemia/reperfusion injury, but the underlying mechanism is unclear. We hypothesized that SPostC protects cardiomyocytes against hypoxia/reoxygenation (H/R) injury by maintaining/restoring mitochondrial morphological integrity, a critical determinant of cell fate.
methodsPrimary cultures of neonatal rat cardiomyocytes (NCMs) were subjected to H/R injury (3 h of hypoxia followed by 3 h reoxygenation). Intervention with SPostC (2.4% sevoflurane) was administered for 15 min upon the onset of reoxygenation. Cell viability, Lactate dehydrogenase (LDH) level, cell death, mitochondrial morphology, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were assessed after intervention. Mitochondrial fusion and fission regulating proteins (Drp1, Fis1, Mfn1, Mfn2 and Opa1) were assessed by immunofluorescence staining and western blotting was performed to determine the level of protein expression.
resultsCardiomyocyte H/R injury resulted in significant increases in LDH release and cell death that were concomitant with reduced cell viability and reduced mitochondrial interconnectivity (mean area/perimeter ratio) and mitochondrial elongation, and with reduced mitochondrial membrane potential and increased mPTP opening. All the above changes were significantly attenuated by SPostC. Furthermore, H/R resulted in significant reductions in mitochondrial fusion proteins Mfn1, Mfn2 and Opa1 and significant enhancement of fission proteins Drp1 and Fis1. SPostC significantly enhanced Mfn2 and Opa1 and reduced Drp1, without significant impact on Mfn1 and Fis1.
conclusionsSevoflurane postconditioning attenuates cardiomyocytes hypoxia/reoxygenation injury (HRI) by restoring mitochondrial fusion/fission balance and morphology.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.