ArticleFrontiers in aging neuroscience2021
Irisin Contributes to Neuroprotection by Promoting Mitochondrial Biogenesis After Experimental Subarachnoid Hemorrhage.
Article 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 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Irisin as an Exerkine of Neuroprotection in Aging and Alzheimer's Disease.Biomolecules · 2026Review
- Irisin as a Regulator of Brain Energy Homeostasis: Implications for Age-Related Neurodegenerative Diseases.Cells · 2026Review
- Application of an intercellular adhesion molecule-1-targeted nanoparticles loaded with irisin in postoperative neurocognitive disorder through metabolic axis activation and barrier restoration.Journal of nanobiotechnology · 2026Article
- Remote Ischemic Preconditioning Exerts Neuroprotective Effects Via the PGC-1α/FNDC5/BDNF Pathway in Focal Brain Ischemia of Rats.Translational stroke research · 2026Article
- Irisin: Emerging Therapeutic Targets for Cognitive Impairment-Related Diseases.Expert reviews in molecular medicine · 2025Review
- Exercise-induced irisin ameliorates cognitive impairment following chronic cerebral hypoperfusion by suppressing neuroinflammation and hippocampal neuronal apoptosis.Journal of neuroinflammation · 2025Article
- Irisin improves ROS‑induced mitohormesis imbalance in H9c2 cells.Molecular medicine reports · 2024Article
- Article
- Somatic BrafAngiogenesis · 2024Article
- The mitochondrial quality control system: a new target for exercise therapeutic intervention in the treatment of brain insulin resistance-induced neurodegeneration in obesity.International journal of obesity (2005) · 2024Review
- Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage.Neural regeneration research · 2024Review
- Rasd1 is involved in white matter injury through neuron-oligodendrocyte communication after subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Inhibition of integrin alpha v/beta 5 mitigates the protective effect induced by irisin in hemorrhage.Experimental and molecular pathology · 2023Article
- The Critical Role of Sirt1 in Subarachnoid Hemorrhages: Mechanism and Therapeutic Considerations.Brain sciences · 2023Review
- Unlocking the Therapeutic Potential of Irisin: Harnessing Its Function in Degenerative Disorders and Tissue Regeneration.International journal of molecular sciences · 2023Review
- Skeletal Muscle Myokine Expression in Critical Illness, Association With Outcome and Impact of Therapeutic Interventions.Journal of the Endocrine Society · 2023Article
- The role of exerkines on brain mitochondria: a mini-review.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Review
- Irisin-Associated Neuroprotective and Rehabilitative Strategies for Stroke.Neuromolecular medicine · 2022Review
- Irisin ameliorates neuroinflammation and neuronal apoptosis through integrin αVβ5/AMPK signaling pathway after intracerebral hemorrhage in mice.Journal of neuroinflammation · 2022Article
- New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.Current neuropharmacology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subarachnoid hemorrhage (SAH) is a devastating form of stroke, which poses a series of intractable challenges to clinical practice. Imbalance of mitochondrial homeostasis has been thought to be the crucial pathomechanism in early brain injury (EBI) cascade after SAH. Irisin, a protein related to metabolism and mitochondrial homeostasis, has been reported to play pivotal roles in post-stroke neuroprotection. However, whether this myokine can exert neuroprotection effects after SAH remains unknown. In the present study, we explored the protective effects of irisin and the underlying mechanisms related to mitochondrial biogenesis in a SAH animal model. Endovascular perforation was used to induce SAH, and recombinant irisin was administered intracerebroventricularly. Neurobehavioral assessments, TdT-UTP nick end labeling (TUNEL) staining, dihydroethidium (DHE) staining, immunofluorescence, western blot, and transmission electron microscopy (TEM) were performed for post-SAH assessments. We demonstrated that irisin treatment improved neurobehavioral scores, reduced neuronal apoptosis, and alleviated oxidative stress in EBI after SAH. More importantly, the administration of exogenous irisin conserved the mitochondrial morphology and promoted mitochondrial biogenesis. The protective effects of irisin were partially reversed by the mitochondrial uncoupling protein-2 (UCP-2) inhibitor. Taken together, irisin may have neuroprotective effects against SAH
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