Carbon Monoxide Alleviates Cardiomyocyte Pyroptosis in Diabetic Cardiomyopathy by Downregulating the IL-33/ST2L Axis

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease Pub Date : 2025-08-23 DOI:10.1002/iid3.70231

Chunjie Jiang, Ping Zhu, Ping Yao, Xiaojun Bi, Chao Gao

{"title":"Carbon Monoxide Alleviates Cardiomyocyte Pyroptosis in Diabetic Cardiomyopathy by Downregulating the IL-33/ST2L Axis","authors":"Chunjie Jiang, Ping Zhu, Ping Yao, Xiaojun Bi, Chao Gao","doi":"10.1002/iid3.70231","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Objectives</h3>\n \n <p>This study aimed to investigate whether carbon monoxide (CO) can alleviate cardiomyocyte pyroptosis by downregulating the IL-33/ST2L axis in diabetic cardiomyopathy (DCM).</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>The diabetic mouse model was established and treated with CO-releasing molecule-2 (CORM-2) or invalid CORM-2 (iCORM-2). For in vitro studies, cardiomyocytes were treated with high glucose (HG).</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>The HG-treated cardiomyocytes exhibited increased IL-33, ST2L, and pyroptosis-related protein expression compared with that in the control group (<i>p</i> < 0.05). Treatment with recombinant IL-33 further increased the expression of HG-induced pyroptosis-related proteins (<i>p</i> < 0.05). Compared with control mice, DCM mice showed reduced cardiac function and elevated expression of IL-33, ST2L, and pyroptosis-related proteins (<i>p</i> < 0.01). Intervention with CORM-2 ameliorated cardiac injury, and decreased the expression of IL-33, ST2L, and pyroptosis-related proteins in vivo and in vitro (<i>p</i> < 0.05). However, iCORM-2 had no effect both in vivo and in vitro.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>In conclusion, CO may inhibit cardiomyocyte pyroptosis by downregulating the IL-33/ST2L axis in DCM mice.</p>\n </section>\n </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 8","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70231","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunity, Inflammation and Disease","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/iid3.70231","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Objectives

This study aimed to investigate whether carbon monoxide (CO) can alleviate cardiomyocyte pyroptosis by downregulating the IL-33/ST2L axis in diabetic cardiomyopathy (DCM).

Methods

The diabetic mouse model was established and treated with CO-releasing molecule-2 (CORM-2) or invalid CORM-2 (iCORM-2). For in vitro studies, cardiomyocytes were treated with high glucose (HG).

Results

The HG-treated cardiomyocytes exhibited increased IL-33, ST2L, and pyroptosis-related protein expression compared with that in the control group (p < 0.05). Treatment with recombinant IL-33 further increased the expression of HG-induced pyroptosis-related proteins (p < 0.05). Compared with control mice, DCM mice showed reduced cardiac function and elevated expression of IL-33, ST2L, and pyroptosis-related proteins (p < 0.01). Intervention with CORM-2 ameliorated cardiac injury, and decreased the expression of IL-33, ST2L, and pyroptosis-related proteins in vivo and in vitro (p < 0.05). However, iCORM-2 had no effect both in vivo and in vitro.

Conclusions

In conclusion, CO may inhibit cardiomyocyte pyroptosis by downregulating the IL-33/ST2L axis in DCM mice.

Abstract Image

查看原文本刊更多论文

一氧化碳通过下调IL-33/ST2L轴减轻糖尿病心肌病心肌细胞焦亡

目的探讨一氧化碳（CO）是否通过下调糖尿病性心肌病（DCM）的IL-33/ST2L轴来缓解心肌细胞焦亡。方法建立糖尿病小鼠模型，用co -释放分子2 （CORM-2）或无效CORM-2 （iCORM-2）治疗。在体外研究中，心肌细胞用高糖（HG）处理。结果与对照组相比，hg处理心肌细胞IL-33、ST2L和焦热相关蛋白表达增加（p < 0.05）。重组IL-33进一步增加了hg诱导的焦热相关蛋白的表达（p < 0.05）。与对照组小鼠相比，DCM小鼠的心功能降低，IL-33、ST2L和焦热相关蛋白的表达升高（p < 0.01）。CORM-2干预改善了心脏损伤，降低了体内和体外IL-33、ST2L和热死相关蛋白的表达（p < 0.05）。然而，iCORM-2在体内和体外均无作用。结论CO可能通过下调IL-33/ST2L轴抑制DCM小鼠心肌细胞焦亡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Immunity, Inflammation and Disease Medicine-Immunology and Allergy

CiteScore

3.60

自引率

0.00%

发文量

146

审稿时长

8 weeks

期刊介绍： Immunity, Inflammation and Disease is a peer-reviewed, open access, interdisciplinary journal providing rapid publication of research across the broad field of immunology. Immunity, Inflammation and Disease gives rapid consideration to papers in all areas of clinical and basic research. The journal is indexed in Medline and the Science Citation Index Expanded (part of Web of Science), among others. It welcomes original work that enhances the understanding of immunology in areas including: • cellular and molecular immunology • clinical immunology • allergy • immunochemistry • immunogenetics • immune signalling • immune development • imaging • mathematical modelling • autoimmunity • transplantation immunology • cancer immunology