ArticleMedical science monitor : international medical journal of experimental and clinical research2020
Inhibition of the Peroxisome Proliferator-Activated Receptor gamma Coactivator 1-alpha (PGC-1α)/Sirtuin 3 (SIRT3) Pathway Aggravates Oxidative Stress After Experimental Subarachnoid Hemorrhage.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- CircRNA circ_0004058 Modulates Early Brain Injury in Subarachnoid Hemorrhage Through miR-221-3p and VE1 Activation Pathway.Translational stroke research · 2025Article
- Irisin protects against cerebral ischemia reperfusion injury in a SIRT3-dependent manner.Frontiers in pharmacology · 2025Article
- Sirtuins as Potential Targets for Neuroprotection: Mechanisms of Early Brain Injury Induced by Subarachnoid Hemorrhage.Translational stroke research · 2024Review
- Mechanism ofFrontiers in pharmacology · 2024Article
- SS31 Confers Cerebral Protection by Reversing Mitochondrial Dysfunction in Early Brain Injury Following Subarachnoid Hemorrhage, via the Nrf2- and PGC-1α-Dependent Pathways.Neurochemical research · 2023Article
- Sirtuin-3: A potential target for treating several types of brain injury.Frontiers in cell and developmental biology · 2023Review
- Role of SIRT3 in neurological diseases and rehabilitation training.Metabolic brain disease · 2023Review
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
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
BACKGROUND Emerging evidence shows that Sirtuin 3 (SIRT3) can exert an antioxidative effect in various neurodegenerative diseases, but whether and how SIRT3 modulates neuronal death after subarachnoid hemorrhage (SAH) remains to be elucidated. MATERIAL AND METHODS Experimental SAH was induced in adult mice by prechiasmatic cistern injection and primary neurons by OxyHb incubation. The peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) and SIRT3 protein levels were examined at different time points after SAH induction. The PGC-1alpha protein gene knockdown in vivo and in vitro was achieved by transfection of lentivirus (LV) vectors expressing shPGC-1alpha or negative control (NC). Western blot, oxidative stress index, histopathology, neurological function, and cell viability analysis was performed. RESULTS Results showed that the PGC-1alpha/SIRT3 pathway was remarkably activated in vivo and in vitro after SAH. LV-shPGC-1alpha treatment significantly inhibited the activation of this pathway after SAH, accompanied by deteriorated neurologic function, aggravated oxidative stress, increased neuronal apoptosis, and enhanced cytotoxicity compared with the mice or primary neurons treated with LV-NC only. CONCLUSIONS The present results highlight the detrimental PGC-1alpha/SIRT3 pathway, involving regulation of the endogenous antioxidant activity against neuronal damage, which may provide a potential therapeutic target in SAH.
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