Evidence map›Paper›PMID 41328028›Full record

ArticleHistology and histopathology2026

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

Xinbin Wang, Guligena Sawuer, Cheng Liang, Lu Lu, Gang Wu

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Article in Histology and histopathology, 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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5 · Who and what money

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5 authors.

Xinbin WangDepartment of Cardiology, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi, Xinjiang, China.
Guligena SawuerDepartment of Cardiology, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi, Xinjiang, China.
Cheng LiangDepartment of Cardiology, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi, Xinjiang, China.
Lu LuDepartment of Cardiology, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi, Xinjiang, China.
Gang WuDepartment of Cardiology, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi, Xinjiang, China. wugang053072@126.com.

Funding

Department of Cardiology, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University
6 · The paper itself

Abstract

backgroundMyocardial 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.

methodsA 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 overexpression 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.

resultsSIRT2 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.

conclusionFOXO3 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.

Indexed as

Forkhead Box Protein O3InflammasomesMyocardial Reperfusion InjuryNLR Family, Pyrin Domain-Containing 3 ProteinSirtuin 2AnimalsDisease Models, AnimalMaleMyocardiumMyocytes, CardiacRatsRats, Sprague-DawleySignal TransductionForkhead Box Protein O3FOXO3 protein, ratInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratSirt2 protein, ratSirtuin 2

Identifiers

PMID41328028

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.