ReviewFrontiers in aging neuroscience2021
Mitochondrial Dynamics: A Potential Therapeutic Target for Ischemic Stroke.
Review in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 80 citations in OpenAlex.
- Mitochondrial targeting strategies for mitigating oxidative damage and enhancing neuroprotection in ischemic stroke: A Review.IBRO neuroscience reports · 2026Review
- Far-infrared irradiation restores mitochondrial dynamics to ameliorate ischemic stroke.Neural regeneration research · 2026Article
- Cell Therapy as Metabolic Rescue after Ischemic Stroke: Rewiring Bioenergetics, Redox Homeostasis, and Neurovascular Repair.Stem cell reviews and reports · 2026Review
- Molecular Drivers of Cognitive Decline and Neuroprotection in Obstructive Sleep Apnea: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Drp1-Dependent Mitochondrial Fission in the Hippocampus Drives Chronic Stress-Induced Depressive-like Behaviors in Mice.International journal of molecular sciences · 2026Article
- Intercellular Mitochondrial Transfer as Endogenous Neuroprotection: Mechanisms and Therapeutic Implications in Ischemic Stroke.Translational stroke research · 2026Review
- Postpartum Plasma-Derived Exosomes Confer Mitochondrial Stabilization and Neuroprotection against Ischemic Stroke.Research square · 2026Article
- Identification of Mitochondrial Dysfunction Genes as Diagnostic Biomarkers for Ischemic Stroke by Integrated Bioinformatics Analysis and Machine Learning.Journal of molecular neuroscience : MN · 2026Article
- Mechanisms and Therapeutic Targets of Ischemia-Reperfusion Injury in Stroke: A Narrative Review Focusing on Blood-Brain Barrier Dysfunction.Brain sciences · 2026Review
- Mitochondria as a therapeutic target in neurodegeneration caused by hypoxia and ischemia during the perinatal period.Pharmacological reports : PR · 2026Review
- pH-sensitive probes for ischemic stroke: advancing early detection and accurate grading.Frontiers in molecular biosciences · 2026Review
- Anti-Inflammatory Mechanisms and Translational Relevance ofJournal of inflammation research · 2026Review
- Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury.Communications biology · 2025Article
- When Mitochondria Falter, the Barrier Fails: Mechanisms of Inner Blood-Retinal Barrier (iBRB) Injury and Opportunities for Mitochondria-Targeted Repair.International journal of molecular sciences · 2025Review
- The AMPK/GDF15 Axis: A Novel Target for the Neuroprotective Effects of Metformin in Ischemic Stroke.Molecular neurobiology · 2025Review
- Mechanistic Insights intoMicroorganisms · 2025Article
- Harnessing Mitochondrial Function for Post-Stroke Rehabilitation: Unlocking Antioxidant Power.Antioxidants (Basel, Switzerland) · 2025Review
- Advances in brain remodeling, stem cell therapies, and translational barriers in stroke and brain aging.Biogerontology · 2025Review
- Buyang Huanwu Decoction improves energy metabolism disorders after cerebral ischemia-reperfusion by regulating the SIRT1/AMPK signaling pathway to promote glycolysis and the tricarboxylic acid cycle.Chinese medicine · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is one of the leading causes of death and disability worldwide. Brain injury after ischemic stroke involves multiple pathophysiological mechanisms, such as oxidative stress, mitochondrial dysfunction, excitotoxicity, calcium overload, neuroinflammation, neuronal apoptosis, and blood-brain barrier (BBB) disruption. All of these factors are associated with dysfunctional energy metabolism after stroke. Mitochondria are organelles that provide adenosine triphosphate (ATP) to the cell through oxidative phosphorylation. Mitochondrial dynamics means that the mitochondria are constantly changing and that they maintain the normal physiological functions of the cell through continuous division and fusion. Mitochondrial dynamics are closely associated with various pathophysiological mechanisms of post-stroke brain injury. In this review, we will discuss the role of the molecular mechanisms of mitochondrial dynamics in energy metabolism after ischemic stroke, as well as new strategies to restore energy homeostasis and neural function. Through this, we hope to uncover new therapeutic targets for the treatment of ischemic stroke.
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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.