ArticleScientific reports2016
Sestrin2 Silencing Exacerbates Cerebral Ischemia/Reperfusion Injury by Decreasing Mitochondrial Biogenesis through the AMPK/PGC-1α Pathway in Rats.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 90 citations in OpenAlex.
- Mitochondrial dysfunction‑driven ferroptosis in cerebral ischemia‑reperfusion injury: Mechanisms and therapeutic strategies (Review).Molecular medicine reports · 2026Review
- Leucine Enhances Stress Resistance in Honeybees (Biology · 2026Article
- Review
- SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Knockdown of SESN2 Exacerbates Cerebral Ischemia-Reperfusion Injury Through Enhancing Glycolysis via the mTOR/HIF-1α Pathway.CNS neuroscience & therapeutics · 2025Article
- Inhibition of MARK4 Promotes Mitochondrial Biogenesis by Inducing the Phosphorylation of AMPKα to Reduce Myocardial Damage in Rats With Myocardial Infarction.Cardiology research and practice · 2025Article
- SESN2 attenuates sevoflurane-induced cognitive impairment and neuroinflammation in rats.Experimental brain research · 2024Article
- Protopine Exerts Neuroprotective Effects on Neonatal Hypoxic-Ischemic Brain Damage in Rats via Activation of the AMPK/PGC1α Pathway.Drug design, development and therapy · 2024Article
- The effects of whole-body vibration therapy on immune and brain functioning: current insights in the underlying cellular and molecular mechanisms.Frontiers in neurology · 2024Review
- The mitochondria as a potential therapeutic target in cerebral I/R injury.Frontiers in neuroscience · 2024Review
- Based on bioinformatics, SESN2 negatively regulates ferroptosis induced by ischemia reperfusion via the System Xc-/GPX4 pathway.Frontiers in genetics · 2024Article
- Amlodipine alleviates renal ischemia/reperfusion injury in rats through Nrf2/Sestrin2/PGC-1α/TFAM Pathway.BMC pharmacology & toxicology · 2023Article
- Neuroprotective Effect of miR-483-5p Against Cardiac Arrest-Induced Mitochondrial Dysfunction Mediated Through the TNFSF8/AMPK/JNK Signaling Pathway.Cellular and molecular neurobiology · 2023Article
- Adenosine receptor A1 enhanced mitochondrial biogenesis and exerted neuroprotection after cerebral ischemia through PGC-1α.Experimental brain research · 2023Article
- Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases.International journal of molecular sciences · 2023Review
- Sestrin2 as a Protective Shield against Cardiovascular Disease.International journal of molecular sciences · 2023Review
- Sestrin2 in diabetes and diabetic complications.Frontiers in endocrinology · 2023Review
- Sestrin2 Signaling Pathway Regulates Podocyte Biology and Protects against Diabetic Nephropathy.Journal of diabetes research · 2023Review
- E3 Ubiquitin Ligase FBXO3 Drives Neuroinflammation to Aggravate Cerebral Ischemia/Reperfusion Injury.International journal of molecular sciences · 2022Article
- Puerarin Attenuates Oxidative Stress and Ferroptosis via AMPK/PGC1α/Nrf2 Pathway after Subarachnoid Hemorrhage in Rats.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sestrin2 (Sesn2) exerts neuroprotective properties in some neurodegenerative diseases. However, the role of Sesn2 in stroke is unclear. The AMP-activated protein kinase/peroxisome proliferator-activated receptor γ coactivator-1α (AMPK/PGC-1α) pathway plays an important role in regulating mitochondrial biogenesis, which helps prevent cerebral ischemia/reperfusion (I/R) injury. Here, we aimed to determine whether Sesn2 alleviated I/R damage by regulating mitochondrial biogenesis through the AMPK/PGC-1α signaling pathway. To be able to test this, Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 1 h with Sesn2 silencing. At 24 h after reperfusion, we found that neurological deficits were exacerbated, infarct volume was enlarged, and oxidative stress and neuronal damage were greater in the Sesn2 siRNA group than in the MCAO group. To explore protective mechanisms, an AMPK activator was used. Expression levels of Sesn2, p-AMPK, PGC-1α, NRF-1, TFAM, SOD2, and UCP2 were significantly increased following cerebral I/R. However, upregulation of these proteins was prevented by Sesn2 small interfering RNA (siRNA). In contrast, activation of AMPK with 5'-aminoimidazole-4-carboxamide riboside weakened the effects of Sesn2 siRNA. These results suggest that Sesn2 silencing may suppress mitochondrial biogenesis, reduce mitochondrial biological activity, and finally aggravate cerebral I/R injury through inhibiting the AMPK/PGC-1α pathway.
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