在糖尿病视网膜病变中,NFAT5-AR轴与高度,功能障碍和与中性粒细胞相关的炎症标记物有关
Fátima Sofía Magaña-Guerrero1, Beatriz Buentello-Volante1, Norma Angélica Magaña-Guerrero1,2
1Cell and Tissue Biology Department, Research Unit, Institute of Ophthalmology Conde de Valenciana Foundation, Cimpalpopoca 14, Mexico City 06800, Mexico.
中性粒细胞中NFAT5-阿尔多减少酶通路的激活与糖尿病视网膜病变 (DR) 的进展有关. 这一途径有助于2型糖尿病 (T2D) 的炎症和超位失衡.
科学领域:
- 内分泌学和新陈代谢学
- 免疫学 免疫学 免疫学
- 眼科医生 眼科 眼科
背景情况:
- 糖尿病视网膜病变 (DR) 是2型糖尿病 (T2D) 的严重并发症,与慢性炎症有关.
- 中性粒细胞,NFAT5和阿尔多减少酶 (AR) 都与DR病理生理学有关.
- NFAT5-AR轴调节索比的积累,可能损害视网膜细胞.
研究的目的:
- 评估具有和没有T2D和DR的个体中性粒细胞中的NFAT5和AR表达.
- 研究NFAT5和AR与T2D-DR中的临床,代谢和炎症标志物的关联.
主要方法:
- 使用ELISA对150名参与者的中性粒细胞 (非糖尿病人,没有DR的T2D,DR的T2D) 量化了NFAT5和AR水平.
- 评估了临床,代谢 (等离子体度),功能 (eGFR) 和炎症标志物 (NLR,NPAR).
主要成果:
- T2D-DR患者的功能受损,血度较高,炎症比率较高.
- 在T2D-DR患者的中性粒细胞中,NFAT5和AR水平显著增加.
- 增加的NFAT5和AR与血度和炎症标志物正相关,与EGFR相反.
结论:
- NFAT5-AR通路在DRT2D患者的中性粒细胞中被激活.
- 这种激活有助于中性粒细胞介导的炎症和hyperosmolar失调.
- NFAT5-AR途径可能是影响DR进展的关键因素.
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