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Inhibiting NLPR3 inflammasome by FOXO3-mediated activation of SIRT2 alleviates myocardial injury in rats

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dc.contributor.authorGuligena Sawuer
dc.contributor.authorCheng Liang
dc.contributor.authorLu Lu
dc.contributor.authorGang Wu
dc.contributor.authorXinbin Wang
dc.contributor.departmentBiología Celular e Histología
dc.contributor.editorUniversidad de Murcia, Departamento de Biologia Celular e Histiologia
dc.date.accessioned2026-05-20T14:50:14Z
dc.date.available2026-05-20T14:50:14Z
dc.date.issued2026
dc.description.abstractBackground. Myocardial ischemia/ reperfusion (MI/R) injury may cause serious arrhythmia and even sudden death. Sirtuin 2 (SIRT2) belongs to NAD (+) dependent class III histone deacetylase. The present study explored the potential mechanism of SIRT2 in MI/R injury. Methods. A rat model with MI/R injury was established. Differentially expressed genes in myocardial tissues of MI/R-treated rats and sham-operated rats were analyzed by microarray. The AAV9-encapsulated SIRT2 overexpression vector was injected into rats to evaluate the effect of SIRT2 on MI/R injury. Oxygen glucose deprivation/reoxygenation (OGD/R) treatment was used to simulate MI/R injury at a cellular level. SIRT2 over expression vector was transfected into cardiomyocytes. The expression of forkhead box O3 (FOXO3), a potential transcription factor predicted to bind to SIRT2, was detected in myocardial tissues of modeled rats and OGD/R-treated cardiomyocytes. The effect of FOXO3 on OGD/R-treated cardiomyocytes was confirmed by functional rescue experiments. The expressions of NLRP3 and caspase1 were detected. Results. SIRT2 was downregulated in myocardial tissues of MI/R-treated rats. Overexpression of SIRT2 alleviated MI/R injury in modeled rats and enhanced viability of OGD/R-treated cardiomyocytes. FOXO3 activated SIRT2 transcription and expression. FOXO3 was downregulated in the myocardial tissues of MI/R treated rats and OGD/R-treated cardiomyocytes. Knockdown of FOXO3 weakened the effects of SIRT2 on MI/R injury. SIRT2 reduced MI/R injury by inhibiting NLPR3/caspase1 inflammasome signaling. Conclusion. FOXO3 activates SIRT2 expression and inhibits NLPR3 inflammasome signaling pathway, thus alleviating MI/R injury. This study may offer a novel molecular target for the management of MI/R injury.
dc.formatapplication/pdf
dc.format.extent14
dc.identifier.doihttps://doi.org/ 10.14670/HH-25-020
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/233501
dc.languageeng
dc.relationSin financiación externa a la Universidad
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectNLPR3 inflammasome
dc.subjectMyocardial ischemia/reperfusion
dc.subjectTranscription factor FOXO3
dc.subjectOxygen glucose deprivation/reoxygenation
dc.subjectSirtuin 2
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleInhibiting NLPR3 inflammasome by FOXO3-mediated activation of SIRT2 alleviates myocardial injury in rats
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublication
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Histology and histopathology, Vol.41, Nº6, (2026)