Almohaimeed Ghada M, Alonazi Asma S, Bin Dayel Anfal F, Alshammari Tahani K, Alghibiwi Hanan K, Alamin Maha A, Almotairi Ahmad R, Alrasheed Nouf M
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Department of Pathology, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia.
Biomedicines. 2024 Mar 29;12(4):759. doi: 10.3390/biomedicines12040759.
Type 2 diabetes mellitus (T2DM) is a critical health problem, with 700 million diagnoses expected worldwide by 2045. Uncontrolled high blood glucose levels can lead to serious complications, including diabetic cardiomyopathy (DCM). Diabetes induces cardiovascular aging and inflammation, increasing cardiomyopathy risk. DCM is characterized by structural and functional abnormalities in the heart. Growing evidence suggests that cellular senescence and macrophage-mediated inflammation participate in the pathogenesis and progression of DCM. Evidence indicates that growth differentiation factor-15 (GDF-15), a protein that belongs to the transforming growth factor-beta (TGF-β) superfamily, is associated with age-related diseases and exerts an anti-inflammatory role in various disease models. Although further evidence suggests that GDF-15 can preserve Klotho, a transmembrane antiaging protein, emerging research has elucidated the potential involvement of GDF-15 and Klotho in the interplay between macrophages-induced inflammation and cellular senescence in the context of DCM. This review explores the intricate relationship between senescence and macrophages in DCM while highlighting the possible contributions of GDF-15 and Klotho.
2型糖尿病（T2DM）是一个严重的健康问题，预计到2045年全球将有7亿例确诊病例。血糖水平控制不佳会导致严重并发症，包括糖尿病性心肌病（DCM）。糖尿病会引发心血管衰老和炎症，增加患心肌病的风险。DCM的特征是心脏结构和功能异常。越来越多的证据表明，细胞衰老和巨噬细胞介导的炎症参与了DCM的发病机制和进展。有证据表明，生长分化因子15（GDF-15）是一种属于转化生长因子-β（TGF-β）超家族的蛋白质，与年龄相关疾病有关，并在各种疾病模型中发挥抗炎作用。尽管进一步的证据表明GDF-15可以保护跨膜抗衰老蛋白α-klotho，但新出现的研究已经阐明了GDF-15和α-klotho在DCM背景下巨噬细胞诱导的炎症与细胞衰老之间相互作用中的潜在作用。这篇综述探讨了DCM中衰老与巨噬细胞之间的复杂关系，同时强调了GDF-15和α-klotho可能的作用。
