Al Madhoun Ashraf
Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15400, Kuwait.
World J Diabetes. 2024 Aug 15;15(8):1654-1658. doi: 10.4239/wjd.v15.i8.1654.
In this editorial, we comment on the article by Zhang . Diabetes mellitus is a chronic disorder associated with several complications like cardiomyopathy, neuropathy, and retinopathy. Diabetes prevalence is increasing worldwide. Multiple diabetes medications are prescribed based on individual patients' needs. However, the exact mechanisms by which many of these drugs exert their pro-tective effects remain unclear. Zhang elucidates molecular mechanisms undelaying cardioprotective effect of the dipeptidyl peptidase-IV inhibitor, teneligliptin. Briefly, teneligliptin alleviates the activation of NOD-like receptor protein 3 inflammasome, a multiprotein complex that plays a pivotal role in regulating the innate immune system and inflammatory signaling. Suppression of NOD-like receptor protein 3 inflammasome activity reduces the expression of cytokines, oxygen radicals and inflammation. These findings highlight teneligliptin as an anti-diabetic cardioprotective reagent.
在这篇社论中,我们对张的文章发表评论。糖尿病是一种与多种并发症相关的慢性疾病,如心肌病、神经病变和视网膜病变。糖尿病在全球的患病率正在上升。多种糖尿病药物是根据个体患者的需求开具的。然而,这些药物中许多发挥其保护作用的确切机制仍不清楚。张阐明了二肽基肽酶-IV抑制剂替格列汀的心脏保护作用的分子机制。简而言之,替格列汀减轻了NOD样受体蛋白3炎性小体的激活,NOD样受体蛋白3炎性小体是一种多蛋白复合物,在调节先天免疫系统和炎症信号中起关键作用。抑制NOD样受体蛋白3炎性小体的活性可降低细胞因子、氧自由基和炎症的表达。这些发现突出了替格列汀作为一种抗糖尿病心脏保护药物的作用。