Mohammadi Saeed, Al-Harrasi Ahmed
Natural and Medical Sciences Research Center, University of Nizwa, Nizwa 616, Oman.
Department of Biological Sciences and Chemistry, University of Nizwa, Nizwa 616, Oman.
World J Diabetes. 2024 Sep 15;15(9):1847-1852. doi: 10.4239/wjd.v15.i9.1847.
This editorial introduces the potential of targeting macrophage function for diabetic cardiomyopathy (DCM) treatment by dipeptidyl peptidase-4 (DPP-4) inhibitors. Zhang studied teneligliptin, a DPP-4 inhibitor used for diabetes management, and its potential cardioprotective effects in a diabetic mouse model. They suggested teneligliptin administration may reverse established markers of DCM, including cardiac hypertrophy and compromised function. It also inhibited the NLRP3 inflammasome and reduced inflammatory cytokine production in diabetic mice. Macrophages play crucial roles in DCM pathogenesis. Chronic hyperglycemia disturbs the balance between pro-inflammatory (M1) and anti-inflammatory (M2) macrophages, favoring a pro-inflammatory state contributing to heart damage. Here, we highlight the potential of DPP-4 inhibitors to modulate macrophage function and promote an anti-inflammatory environment. These compounds may achieve this by elevating glucagon-like peptide-1 levels and potentially inhibiting the NLRP3 inflammasome. Further studies on teneligliptin in combination with other therapies targeting different aspects of DCM could be suggested for developing more effective treatment strategies to improve cardiovascular health in diabetic patients.
这篇社论介绍了二肽基肽酶-4（DPP-4）抑制剂针对糖尿病性心肌病（DCM）治疗靶向巨噬细胞功能的潜力。张研究了用于糖尿病管理的DPP-4抑制剂替格列汀及其在糖尿病小鼠模型中的潜在心脏保护作用。他们认为给予替格列汀可能会逆转已确立的DCM标志物，包括心脏肥大和功能受损。它还抑制了糖尿病小鼠中的NLRP3炎性小体并减少了炎性细胞因子的产生。巨噬细胞在DCM发病机制中起关键作用。慢性高血糖会扰乱促炎（M1）和抗炎（M2）巨噬细胞之间的平衡，有利于导致心脏损伤的促炎状态。在此，我们强调DPP-4抑制剂调节巨噬细胞功能并促进抗炎环境的潜力。这些化合物可能通过提高胰高血糖素样肽-1水平并可能抑制NLRP3炎性小体来实现这一点。可以建议对替格列汀与针对DCM不同方面的其他疗法联合进行进一步研究，以制定更有效的治疗策略，改善糖尿病患者的心血管健康。
