ArticleMolecular biology reports2026
Sevoflurane suppresses circ_SMG6 to inhibit TLR4/mTOR signaling and attenuate myocardial ischemia-reperfusion injury.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMyocardial ischemia-reperfusion injury (MIRI) is a main contributor to adverse effects after acute myocardial infarction. Sevoflurane provides cardioprotection, however the link of role Sevoflurane with circular RNAs, particularly circ_SMG6, and interaction with TLR4/mTOR signaling is unknown.
methodsSprague-Dawley rats were divided into Sham, MIRI, or sevoflurane+MIRI groups and the Myocardial infarct size, histopathology, and myocardial apoptotic nuclei in rat hearts were measured by 2,3,5-Triphenyltetrazolium Chloride (TTC) staining, Hematoxylin and Eosin (H&E), and TUNEL staining. Additionally, circ_SMG6 and TLR4/mTOR expression were quantified by qRT-PCR and Western blotting. In order to assess viability, apoptosis, inflammatory cytokines, and TLR4/mTOR signaling readout, human cardiomyocytes were transfected with circ_SMG6 overexpression or knockdown vectors 48 h before hypoxia-reoxygenation (H/R) induction, either with or without sevoflurane.
resultsMIRI increased the myocardial apoptotic index, infarct size, and structural cardiac damage with elevated circ_SMG6 and TLR4/mTOR signaling. These alterations were lessened with sevoflurane, although they were not entirely restored. H/R increased circ_SMG6, improved TLR4/mTOR signaling readout, reduced viability, and increased TNF α/IL 1β/IL 6 production in AC16 and HCM cells. circ_SMG6 knockdown reversed these effects, whereas circ_SMG6 overexpression further aggravated H/R-induced injury, supporting the functional involvement of circ_SMG6 in TLR4/mTOR-associated inflammatory and apoptotic responses. Sevoflurane treatment phenocopied circ_SMG6 silencing at both functional and signaling levels.
conclusionscirc_SMG6 may exacerbate MIRI through TLR4/mTOR-associated inflammatory and apoptotic signaling in cardiomyocytes, while sevoflurane attenuates myocardial injury, at least in part, by suppressing this circ_SMG6-related pathway. These findings identify circ_SMG6 as a potential therapeutic target in sevoflurane-based cardioprotection against MIRI.
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