ArticleCellular and molecular neurobiology2020
TGF-β3/Smad3 Contributes to Isoflurane Postconditioning Against Cerebral Ischemia-Reperfusion Injury by Upregulating MEF2C.
Article in Cellular and molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Engineering RVG-modified exosomes for targeting TGF-β1 signaling in stroke recovery.Journal of translational medicine · 2026Article
- Metformin attenuates diabetic osteoporosis via the miR-21 mediated Mef2c/Sost pathway.Frontiers in endocrinology · 2026Article
- TGF-β3 Protects Neurons Against Intermittent Hypoxia-Induced Oxidative Stress and Apoptosis Through Activation of the Nrf-2/KEAP1/HO-1 Pathway via Binding to TGF-βRI.Neurochemical research · 2023Article
- Isoflurane Enhances Autophagy by Activating AMPK/ULK1, Inhibits NLRP3, and Reduces Cognitive Impairment After Cerebral Ischemia-Reperfusion Injury in Rats.Journal of molecular neuroscience : MN · 2023Article
- The protective effects of lncRNA ZFAS1/miR-421-3p/MEF2C axis on cerebral ischemia-reperfusion injury.Cell cycle (Georgetown, Tex.) · 2022Article
- Protective effect of isoflurane preconditioning on neurological function in rats with HIE.Ibrain · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
Isoflurane postconditioning alleviates cerebral ischemic-reperfusion injury (CIRI), but the underlying mechanism has not been fully clarified. We previously demonstrated that the transforming growth factor beta-1 (TGF-β1)/Smads signaling pathway is involved in the neuroprotective effect of isoflurane postconditioning. TGF-β3 has a highly homologous sequence relative to that of TGF-β1. In this study, we explored the roles of the TGF-β3/Smad3 signaling pathway and myocyte enhancer factor 2C (MEF2C) in neuroprotection induced by isoflurane postconditioning. A CIRI rat model was established by middle cerebral artery occlusion for 1.5 h, followed by 24 h of reperfusion. Isoflurane postconditioning led to lower infarct volumes and neurologic deficit scores, more surviving neurons, and less damaged and apoptotic neurons as compared with those of CIRI rats. Moreover, isoflurane postconditioning upregulated the expressions of TGF-β3, p-Smad3, and MEF2C. However, the neuroprotective effect was reversed by pirfenidone, a TGF-β3/Smad3 signaling pathway inhibitor. Also, pirfenidone treatment downregulated the expression of MEF2C. These results indicate that the TGF-β3/Smad3 signaling pathway contributes to the neuroprotection of isoflurane postconditioning after CIRI and is possibly related to MEF2C.
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