ArticleMolecular and cellular neurosciences2016
Mitochondrial dynamics following global cerebral ischemia.
Article in Molecular and cellular neurosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 96 citations in OpenAlex.
- Modeling Hemorrhagic Shock in Male SD Rats by Fixed Volume Blood Withdrawal Followed by Partial Resuscitation and Long-Term Outcome Assessment.Medical sciences (Basel, Switzerland) · 2026Article
- Cortistatin as a modulator of inflammatory and mitochondrial dysfunction in Huntington´s disease.Journal of neuroinflammation · 2026Article
- Recent Advances in Mitochondrial Transplantation for Ischemic Stroke: A Review of in Vitro and in Vivo Studies.Translational stroke research · 2026Review
- The role of mitochondrial dynamics in metabolic dysfunction-associated steatotic liver disease.Frontiers in medicine · 2026Review
- Deep learning analysis of urine-derived stem cell mitochondrial morphology as a non-invasive Alzheimer's disease biomarker.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Pituitary adenylate cyclase-activating polypeptide and mitochondrial homeostasis in neuronal injury: mechanisms and translational prospects.Frontiers in immunology · 2026Review
- Protein Phosphatase 1 Regulatory Subunit 17 (PPP1R17) Regulates Cerebral Ischemia and Ischemia-Reperfusion Brain Injury by Suppressing YAP1-Mediated Mitophagy.Molecular neurobiology · 2025Article
- Inhibitory Infrared Light Attenuates Mitochondrial Hyperactivity and Accelerates Restoration of Mitochondrial Homeostasis in an Oxygen-Glucose Deprivation/Reoxygenation Model.Antioxidants (Basel, Switzerland) · 2025Article
- The role of cardiolipin in mitochondrial dynamics and quality control in neuronal ischemia/reperfusion injury.Cell death & disease · 2025Review
- Agent-based modeling of neuronal mitochondrial dynamics using intrinsic variables of individual mitochondria.iScience · 2025Article
- Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025Review
- Acupuncture for cognitive impairment in type 2 diabetes mellitus: a systematic review and Bayesian network meta-analysis protocol.Frontiers in medicine · 2025Article
- Mitochondrial membrane potential and oxidative stress interact to regulate Oma1-dependent processing of Opa1 and mitochondrial dynamics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Review
- Organ-Specific Mitochondrial Alterations Following Ischemia-Reperfusion Injury in Post-Cardiac Arrest Syndrome: A Comprehensive Review.Life (Basel, Switzerland) · 2024Review
- Mitochondrial pathways of copper neurotoxicity: focus on mitochondrial dynamics and mitophagy.Frontiers in molecular neuroscience · 2024Review
- MAM-mediated mitophagy and endoplasmic reticulum stress: the hidden regulators of ischemic stroke.Frontiers in cellular neuroscience · 2024Review
- Review
- Ginsenoside compound K protects against cerebral ischemia/reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy.Journal of ginseng research · 2023Article
- Asialo-rhuEPO as a Potential Neuroprotectant for Ischemic Stroke Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Global brain ischemia/reperfusion induces neuronal damage in vulnerable brain regions, leading to mitochondrial dysfunction and subsequent neuronal death. Induction of neuronal death is mediated by release of cytochrome c (cyt c) from the mitochondria though a well-characterized increase in outer mitochondrial membrane permeability. However, for cyt c to be released it is first necessary for cyt c to be liberated from the cristae junctions which are gated by Opa1 oligomers. Opa1 has two known functions: maintenance of the cristae junction and mitochondrial fusion. These roles suggest that Opa1 could play a central role in both controlling cyt c release and mitochondrial fusion/fission processes during ischemia/reperfusion. To investigate this concept, we first utilized in vitro real-time imaging to visualize dynamic changes in mitochondria. Oxygen-glucose deprivation (OGD) of neurons grown in culture induced a dual-phase mitochondrial fragmentation profile: (i) fragmentation during OGD with no apoptosis activation, followed by fusion of mitochondrial networks after reoxygenation and a (ii) subsequent extensive fragmentation and apoptosis activation that preceded cell death. We next evaluated changes in mitochondrial dynamic state during reperfusion in a rat model of global brain ischemia. Evaluation of mitochondrial morphology with confocal and electron microscopy revealed a similar induction of fragmentation following global brain ischemia. Mitochondrial fragmentation aligned temporally with specific apoptotic events, including cyt c release, caspase 3/7 activation, and interestingly, release of the fusion protein Opa1. Moreover, we uncovered evidence of loss of Opa1 complexes during the progression of reperfusion, and electron microscopy micrographs revealed a loss of cristae architecture following global brain ischemia. These data provide novel evidence implicating a temporal connection between Opa1 alterations and dysfunctional mitochondrial dynamics following global brain ischemia.
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Registered trials
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.