{"title":"维拉帕米:治疗1型糖尿病的一个有希望的选择?","authors":"Domina Petric","doi":"10.53388/pr202303011","DOIUrl":null,"url":null,"abstract":"Type 1A diabetes mellitus (DMT1 in the following text) is caused by the autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans [1, 2]. This destruction is determined by genetic susceptibility, such as the presence of HLA-DQalpha, HLA-DQbeta, HLA-DR, preproinsulin, PTPN22 gene, CTLA-4, interferon-induced helicase, IL2 receptor (CD25), lectin-like gene (KIAA0035), and ERBB3e [3–8]. It is usually triggered by environmental agents, such as perinatal factors (maternal age over 25 years, preeclampsia, neonatal respiratory disease, and jaundice), viruses (Coxsackie virus, enteroviruses), dietary factors (cow’s milk), exposure to nitrates, and treatment with checkpoint inhibitors [9–14]. Despite significant improvements in insulin therapy, DMT1 remains a therapeutic challenge. Therefore, the slowing down of pancreatic beta cell (PβC) loss may be of great value. With that said, the author summarizes the available evidence on such therapeutic options.","PeriodicalId":69244,"journal":{"name":"TMR药理学研究","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Verapamil: a promising therapeutic option in diabetes mellitus type 1?\",\"authors\":\"Domina Petric\",\"doi\":\"10.53388/pr202303011\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Type 1A diabetes mellitus (DMT1 in the following text) is caused by the autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans [1, 2]. This destruction is determined by genetic susceptibility, such as the presence of HLA-DQalpha, HLA-DQbeta, HLA-DR, preproinsulin, PTPN22 gene, CTLA-4, interferon-induced helicase, IL2 receptor (CD25), lectin-like gene (KIAA0035), and ERBB3e [3–8]. It is usually triggered by environmental agents, such as perinatal factors (maternal age over 25 years, preeclampsia, neonatal respiratory disease, and jaundice), viruses (Coxsackie virus, enteroviruses), dietary factors (cow’s milk), exposure to nitrates, and treatment with checkpoint inhibitors [9–14]. Despite significant improvements in insulin therapy, DMT1 remains a therapeutic challenge. Therefore, the slowing down of pancreatic beta cell (PβC) loss may be of great value. With that said, the author summarizes the available evidence on such therapeutic options.\",\"PeriodicalId\":69244,\"journal\":{\"name\":\"TMR药理学研究\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"TMR药理学研究\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.53388/pr202303011\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"TMR药理学研究","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.53388/pr202303011","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Verapamil: a promising therapeutic option in diabetes mellitus type 1?
Type 1A diabetes mellitus (DMT1 in the following text) is caused by the autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans [1, 2]. This destruction is determined by genetic susceptibility, such as the presence of HLA-DQalpha, HLA-DQbeta, HLA-DR, preproinsulin, PTPN22 gene, CTLA-4, interferon-induced helicase, IL2 receptor (CD25), lectin-like gene (KIAA0035), and ERBB3e [3–8]. It is usually triggered by environmental agents, such as perinatal factors (maternal age over 25 years, preeclampsia, neonatal respiratory disease, and jaundice), viruses (Coxsackie virus, enteroviruses), dietary factors (cow’s milk), exposure to nitrates, and treatment with checkpoint inhibitors [9–14]. Despite significant improvements in insulin therapy, DMT1 remains a therapeutic challenge. Therefore, the slowing down of pancreatic beta cell (PβC) loss may be of great value. With that said, the author summarizes the available evidence on such therapeutic options.