Verapamil: a promising therapeutic option in diabetes mellitus type 1?

Domina Petric
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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.
维拉帕米:治疗1型糖尿病的一个有希望的选择?
1A型糖尿病(下文简称DMT1)是由朗格汉斯胰岛中产生胰岛素的β细胞的自身免疫破坏引起的[1,2]。这种破坏是由遗传易感性决定的,如hla - dqα、hla - dqβ、HLA-DR、胰岛素前原、PTPN22基因、CTLA-4、干扰素诱导解旋酶、il - 2受体(CD25)、凝集素样基因(KIAA0035)和ERBB3e[3-8]。它通常由环境因素引发,如围产期因素(母亲年龄超过25岁、先兆子痫、新生儿呼吸系统疾病和黄疸)、病毒(柯萨奇病毒、肠道病毒)、饮食因素(牛奶)、硝酸盐暴露和检查点抑制剂治疗[9-14]。尽管胰岛素治疗取得了重大进展,但DMT1仍然是一个治疗挑战。因此,减缓胰腺β细胞(PβC)的损失可能具有重要价值。综上所述,作者总结了这种治疗选择的现有证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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