{"title":"1型糖尿病ß细胞功能障碍的分子和炎症病因。","authors":"Cameron R Rostron, Carmella Evans-Molina","doi":"10.1152/physiol.00008.2025","DOIUrl":null,"url":null,"abstract":"<p><p>Type 1 diabetes (T1D) is a metabolic disease caused by the autoimmune-mediated destruction of pancreatic β cells; however, recent findings indicate that intrinsic stress pathways within β cells may contribute to the initiation or perpetuation of autoimmunity. Here, we discuss the molecular and inflammatory etiologies of β cell dysfunction in T1D, with a focus on cytokine signaling, endoplasmic reticulum stress, mitochondrial dysfunction, and senescence.</p>","PeriodicalId":520753,"journal":{"name":"Physiology (Bethesda, Md.)","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Molecular and Inflammatory Etiologies of ß Cell Dysfunction in Type 1 Diabetes.\",\"authors\":\"Cameron R Rostron, Carmella Evans-Molina\",\"doi\":\"10.1152/physiol.00008.2025\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Type 1 diabetes (T1D) is a metabolic disease caused by the autoimmune-mediated destruction of pancreatic β cells; however, recent findings indicate that intrinsic stress pathways within β cells may contribute to the initiation or perpetuation of autoimmunity. Here, we discuss the molecular and inflammatory etiologies of β cell dysfunction in T1D, with a focus on cytokine signaling, endoplasmic reticulum stress, mitochondrial dysfunction, and senescence.</p>\",\"PeriodicalId\":520753,\"journal\":{\"name\":\"Physiology (Bethesda, Md.)\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-05-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Physiology (Bethesda, Md.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1152/physiol.00008.2025\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Physiology (Bethesda, Md.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1152/physiol.00008.2025","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Molecular and Inflammatory Etiologies of ß Cell Dysfunction in Type 1 Diabetes.
Type 1 diabetes (T1D) is a metabolic disease caused by the autoimmune-mediated destruction of pancreatic β cells; however, recent findings indicate that intrinsic stress pathways within β cells may contribute to the initiation or perpetuation of autoimmunity. Here, we discuss the molecular and inflammatory etiologies of β cell dysfunction in T1D, with a focus on cytokine signaling, endoplasmic reticulum stress, mitochondrial dysfunction, and senescence.