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连接2型糖尿病与心血管并发症的免疫失调

Immune Dysregulation Connecting Type 2 Diabetes and Cardiovascular Complications.

作者信息

Deck Katherine, Mora Christoph, Deng Shuoqiu, Rogers Pamela, Rafferty Tonya, Palade Philip T, Mu Shengyu, Liu Yunmeng

机构信息

Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

出版信息

Life (Basel). 2025 Aug 5;15(8):1241. doi: 10.3390/life15081241.

DOI:10.3390/life15081241
PMID:40868889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12387400/
Abstract

Type 2 diabetes (T2D) is a prevalent metabolic disorder characterized by persistent hyperglycemia, hyperinsulinemia, and long-term cardiovascular complications. Another hallmark of T2D is disrupted hormonal homeostasis-marked by elevated levels of insulin and leptin and reduced adiponectin-which plays a crucial role in modulating immune cell function. Individuals with T2D exhibit a skewed immune profile, with an elevated secretion of pro-inflammatory cytokines such as IFN-γ, TNF-α, IL17, and IL6, which are well-established drivers of vascular inflammation and dysfunction. Moreover, dysregulated metabolic hormones in T2D promote the acquisition of a pro-inflammatory phenotype in immune cells, suggesting that these hormones not only regulate energy balance but also serve as potent immune activators. Their dysregulation likely plays a significant-and perhaps underappreciated-role in the onset and progression of diabetic cardiovascular complications.

摘要

2型糖尿病(T2D)是一种常见的代谢紊乱疾病,其特征为持续性高血糖、高胰岛素血症以及长期的心血管并发症。T2D的另一个标志是激素稳态失调,表现为胰岛素和瘦素水平升高,脂联素水平降低,这在调节免疫细胞功能中起关键作用。T2D患者呈现出免疫谱异常,促炎细胞因子如IFN-γ、TNF-α、IL17和IL6的分泌增加,这些细胞因子是血管炎症和功能障碍的公认驱动因素。此外,T2D中代谢激素失调促使免疫细胞获得促炎表型,这表明这些激素不仅调节能量平衡,还作为强效免疫激活剂发挥作用。它们的失调可能在糖尿病心血管并发症的发生和发展中起重要作用,或许尚未得到充分认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/6cab1a95292c/life-15-01241-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/776a07002521/life-15-01241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/bbf81c810c26/life-15-01241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/3ebf44e2a0b7/life-15-01241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/6cab1a95292c/life-15-01241-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/776a07002521/life-15-01241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/bbf81c810c26/life-15-01241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/3ebf44e2a0b7/life-15-01241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b8/12387400/6cab1a95292c/life-15-01241-g004.jpg

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Leptin Enhances M1 Macrophage Polarization and Impairs Tendon-Bone Healing in Rotator Cuff Repair: A Rat Model.瘦素增强M1巨噬细胞极化并损害肩袖修复中肌腱-骨愈合:大鼠模型
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