ReviewFrontiers in aging neuroscience2020
Mitochondria: Novel Mechanisms and Therapeutic Targets for Secondary Brain Injury After Intracerebral Hemorrhage.
Review in Frontiers in aging neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Perihematomal Edema and Clinical Outcome After Intracerebral Hemorrhage: A Systematic Review and Meta-Analysis.Neurocritical care · 2022Pooled it
- Association of Angiotensin Inhibitors with Improved Outcome after Acute Intracerebral Hemorrhage: Secondary Analysis of the INTERACT3 Trial.Cerebrovascular diseases (Basel, Switzerland) · 2026Trial
- Lactylation and N6-Methyladenosine RNA modification in neuropsychiatric sequelae after intracerebral hemorrhage: a hypothesis-generating metabolic-glial-circuit framework.Molecular biology reports · 2026Review
- [Deubiquitinase USP30 alleviates brain injury after intracerebral hemorrhage by regulating MFN2 ubiquitination].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Mesenchymal Stem Cell-derived Exosomes Alleviate Oxidative Stress and Brain Injuries Through Promoting OPA1 Mediated Mitochondrial Fusion After Intracerebral Hemorrhage.Molecular neurobiology · 2026Article
- α-tocopherol alleviates ketamine toxicity in rat brain neurons.BMC pharmacology & toxicology · 2026Article
- Iron-driven secondary injury after intracranial hemorrhage: mitochondrial dysfunction and ferroptosis.Frontiers in neuroscience · 2026Review
- Mitophagy in Brain Injuries: Mechanisms, Roles, and Therapeutic Potential.Molecular neurobiology · 2025Review
- GPR39 Agonist TC-G 1008 Promoted Mitochondrial Biogenesis and Improved Antioxidative Capability via CREB/PGC-1α Pathway Following Intracerebral Hemorrhage in Mice.Translational stroke research · 2025Article
- The role of potential oxidative biomarkers in the prognosis of intracerebral hemorrhage and the exploration antioxidants as possible preventive and treatment options.Frontiers in molecular biosciences · 2025Review
- Transient receptor potential vanilloid 1 inhibition reduces brain damage by suppressing neuronal apoptosis after intracerebral hemorrhage.Brain pathology (Zurich, Switzerland) · 2024Article
- Celastrol Ameliorates Neuronal Mitochondrial Dysfunction Induced by Intracerebral Hemorrhage via Targeting cAMP-Activated Exchange Protein-1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Iron/ROS/Itga3 mediated accelerated depletion of hippocampal neural stem cell pool contributes to cognitive impairment after hemorrhagic stroke.Redox biology · 2024Article
- Focusing on mitochondria in the brain: from biology to therapeutics.Translational neurodegeneration · 2024Review
- Article
- Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation.Life (Basel, Switzerland) · 2024Review
- Mitochondrial stress: a key role of neuroinflammation in stroke.Journal of neuroinflammation · 2024Review
- Article
- FGF21 alleviates endothelial mitochondrial damage and prevents BBB from disruption after intracranial hemorrhage through a mechanism involving SIRT6.Molecular medicine (Cambridge, Mass.) · 2023Article
- MSCs overexpressing GDNF restores brain structure and neurological function in rats with intracerebral hemorrhage.Molecular biomedicine · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) is a destructive form of stroke that often results in death or disability. However, the survivors usually experience sequelae of neurological impairments and psychiatric disorders, which affect their daily functionality and working capacity. The recent MISTIE III and STICH II trials have confirmed that early surgical clearance of hematomas does not improve the prognosis of survivors of ICH, so it is vital to find the intervention target of secondary brain injury (SBI) after ICH. Mitochondrial dysfunction, which may be induced by oxidative stress, neuroinflammation, and autophagy, among others, is considered to be a novel pathological mechanism of ICH. Moreover, mitochondria play an important role in promoting neuronal survival and improving neurological function after a hemorrhagic stroke. This review summarizes the mitochondrial mechanism involved in cell death, reactive oxygen species (ROS) production, inflammatory activation, blood-brain barrier (BBB) disruption, and brain edema underlying ICH. We emphasize the potential of mitochondrial protection as a potential therapeutic target for SBI after stroke and provide valuable insight into clinical strategies.
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