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<p>NLRP12 can induce PANoptosis, a novel form of inflammatory cell death. The research aimed to investigate the mechanisms of NLRP12 in regulating PANoptosis during postinfarction heart failure (HF). C57BL/6J mice were treated with AAV-shNLRP12 before acute myocardial infarction (AMI) modeling using coronary artery ligation, and mouse cardiomyocytes were treated with lentiviruses before hypoxia. NLRP12 and FOSL2 were upregulated in myocardial tissues of AMI-induced mice and hypoxia-exposed mouse cardiomyocytes. FOSL2 activated NLRP12 in mouse cardiomyocytes by binding to its promoter. Knockdown of FOSL2 or NLRP12 improved survival and inhibited HF after AMI, including recovery of cardiac function, reduction of fibrotic area of myocardial tissues, decrease of myocardial injury, and inhibition of PANoptosis in mice. Combined overexpression of NLRP12 impaired the inhibitory effect of the knockdown of FOSL2 on HF after AMI. Our findings demonstrate that FOSL2 promotes cardiomyocyte PANoptosis by inducing the transcription of NLRP12, thereby triggering HF after AMI.</p>

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FOSL2 Regulates PANoptosis in Cardiomyocytes and Heart Failure Progression After Acute Myocardial Infarction by Promoting NLRP12

  • 期刊论文

  • 发表日期：

    2026年7月28日

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  • Renlian Gu,
  • Yan Sun

摘要

NLRP12 can induce PANoptosis, a novel form of inflammatory cell death. The research aimed to investigate the mechanisms of NLRP12 in regulating PANoptosis during postinfarction heart failure (HF). C57BL/6J mice were treated with AAV-shNLRP12 before acute myocardial infarction (AMI) modeling using coronary artery ligation, and mouse cardiomyocytes were treated with lentiviruses before hypoxia. NLRP12 and FOSL2 were upregulated in myocardial tissues of AMI-induced mice and hypoxia-exposed mouse cardiomyocytes. FOSL2 activated NLRP12 in mouse cardiomyocytes by binding to its promoter. Knockdown of FOSL2 or NLRP12 improved survival and inhibited HF after AMI, including recovery of cardiac function, reduction of fibrotic area of myocardial tissues, decrease of myocardial injury, and inhibition of PANoptosis in mice. Combined overexpression of NLRP12 impaired the inhibitory effect of the knockdown of FOSL2 on HF after AMI. Our findings demonstrate that FOSL2 promotes cardiomyocyte PANoptosis by inducing the transcription of NLRP12, thereby triggering HF after AMI.