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作为一个潜在的病理生理因素,FGF23在与慢性病相关的外周动脉疾病
Javier Donate-Correa1,2,3,4, Ernesto Martín-Núñez1,5, Carolina Hernández-Carballo1
1Research Unit, University Hospital Nuestra Señora de Candelaria (UHNSC), 38010 Santa Cruz de Tenerife, Spain.
International journal of molecular sciences
|May 25, 2024
概括
纤维细胞生长因子23 (FGF23) 与患有外周动脉疾病 (PAD) 的慢性病 (CKD) 患者的炎症有关. 较高的FGF23与血液和组织中瘤亡因子-α (TNFα) 的增加相关.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 心血管医学 心血管医学
- 免疫学 免疫学 免疫学
背景情况:
- 纤维细胞生长因子23 (FGF23) 和炎症在慢性病 (CKD) 中升高,导致疾病进展和并发症.
- 一个FGF23-炎症相互作用可能会创建一个有害的反循环,增加心血管疾病和死亡的风险.
- 周围动脉疾病 (PAD) 与CKD有着异性炎症的基础,这使得它成为研究FGF23.23的相关背景.
研究的目的:
- 为了研究患有PAD的CKD患者的循环FGF23水平.
- 检查FGF23与血清和周围血液循环细胞 (PBCCs) 中的炎症标记物 (TNFα,IL-6,IL-10,CRP,SII,NLR) 之间的关联.
- 评估FGF23和血管TNFα表达之间的关系.
主要方法:
- 测量血清FGF23,TNFα,IL-6,IL-10,CRP,SII和NLR在CKD阶段的3-4个接受关节切除术的患者中.
- 在PBCCs和大腿血管组织中分析了TNFα,IL-6,IL-10和ADAM17的基因表达.
- 在患者子组中确定了血管TNFα蛋白免疫活性.
主要成果:
- FGF23度与TNFα的血清和PBCCmRNA水平独立相关.
- 较差的功能和糖尿病被确定为导致FGF23.23升高的因素.
- 较高的FGF23水平与血管TNFα免疫活性增加相关.
结论:
- 在患有PAD的CKD患者中,FGF23与TNFα驱动的炎症密切相关.
- 功能和糖尿病显著影响FGF23水平.
- 在CKD中,FGF23可能在PAD特征的血管炎症过程中发挥作用.
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