Dobriceanu Roxana-Cristina, Meca Andreea Daniela, Boboc Ianis Kevyn Stefan, Mititelu-Tartau Liliana, Naidin Mihaela Simona, Turcu-Stiolica Adina, Bogdan Maria
Doctoral School, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.
Department of Pharmacology, Faculty of Pharmacy, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.
Biomedicines. 2025 Apr 7;13(4):891. doi: 10.3390/biomedicines13040891.
Diabetes mellitus (DM) is a multifactorial metabolic disorder associated with systemic inflammation and vascular complications. Pentraxin-3 (PTX3) has emerged as a key biomarker of inflammation and endothelial dysfunction in DM. We aimed to examine the role of PTX3 in DM and assesses the impact of pharmacological interventions on its expression. The review included studies analyzing PTX3 modulation by antidiabetic therapies, such as sodium-glucose cotransporter-2 inhibitors (SGLT-2i), glucagon-like peptide-1 agonists (GLP-1a), and dipeptidyl peptidase-4 inhibitors (DPP-4i), as well as the effects of lifestyle interventions. Clinical and experimental studies demonstrated a strong correlation between PTX3 levels and DM progression. Elevated PTX3 levels were associated with diabetic complications, including nephropathy, retinopathy, and cardiovascular diseases. Antidiabetic drugs showed differential effects on PTX3 expression, with GLP-1a and DPP-4i significantly reducing PTX3 levels, while SGLT-2i displayed a paradoxical increase. Lifestyle interventions, including dietary modifications and weight loss, yielded inconsistent effects, suggesting genetic and metabolic factors influence PTX3 regulation. While pharmacological therapies, particularly GLP-1a and DPP-4i, demonstrate anti-inflammatory effects, further research is needed to standardize PTX3 measurement and explore its potential as a therapeutic target. Personalized treatment strategies incorporating genetic profiling may optimize inflammation control and disease management in DM patients.
糖尿病(DM)是一种与全身炎症和血管并发症相关的多因素代谢紊乱疾病。五聚体蛋白3(PTX3)已成为糖尿病炎症和内皮功能障碍的关键生物标志物。我们旨在研究PTX3在糖尿病中的作用,并评估药物干预对其表达的影响。该综述纳入了分析抗糖尿病疗法(如钠-葡萄糖协同转运蛋白2抑制剂(SGLT-2i)、胰高血糖素样肽1激动剂(GLP-1a)和二肽基肽酶4抑制剂(DPP-4i))对PTX3调节作用的研究,以及生活方式干预的效果。临床和实验研究表明PTX3水平与糖尿病进展之间存在密切相关性。PTX3水平升高与糖尿病并发症相关,包括肾病、视网膜病变和心血管疾病。抗糖尿病药物对PTX3表达显示出不同的影响,GLP-1a和DPP-4i可显著降低PTX3水平,而SGLT-2i则出现了矛盾的升高。包括饮食调整和体重减轻在内的生活方式干预产生的效果不一致,表明遗传和代谢因素会影响PTX3的调节。虽然药物治疗,特别是GLP-1a和DPP-4i,显示出抗炎作用,但仍需要进一步研究来规范PTX3的测量,并探索其作为治疗靶点的潜力。纳入基因谱分析的个性化治疗策略可能会优化糖尿病患者的炎症控制和疾病管理。