{"title":"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","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":"{\"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}","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}
Carbon Monoxide Alleviates Cardiomyocyte Pyroptosis in Diabetic Cardiomyopathy by Downregulating the IL-33/ST2L Axis
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.
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
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