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MCP1逆转了FGF23和欧米茄6/3比率之间的相关性:这是否也适用于移植?

Deborah Mattinzoli¹, Stefano Turolo², Masami Ikehata¹

¹Renal Research Laboratory, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy.

Journal of clinical medicine

|September 28, 2023

概括

纤维细胞生长因子 (FGF23) 在移植 (KTx) 患者中增加,但单细胞化学吸引蛋白1 (MCP1) 水平下降. 多不和脂肪酸 (PUFA) 概况发生变化,在KTx患者中观察到较低的n-6/n-3比率.

科学领域:

腎臟病學 (nephrology) 是一種醫學.
生物化学生物化学
免疫学免疫学免疫学

背景情况:

纤维细胞生长因子 (FGF23) 在慢性病 (CKD) 进展期间增加.
在晚期CKD中,FGF23和omega-6 (n-6) 多不和脂肪酸 (PUFA) 之间的正相关性出现.
以前的研究探讨了FGF23和单细胞化学吸引蛋白1 (MCP1) 在CKD相关的脂质不良和心血管风险中的作用.

研究的目的:

在移植 (KTx) 患者中重新评估FGF23,MCP1和PUFA之间的关系.
为了研究这些关系的潜在修改,由于特定于KTx队列的因素.
了解免疫抑制对这些生物标志物的影响.

主要方法:

研究了40名移植患者 (KTx).
使用ELISA和气体染色学评估MCP1,FGF23和PUFA水平.
分析了FGF23,MCP1和各种n-6和n-3PUFA之间的相关性.

主要成果:

在KTx患者中,FGF23水平显著增加 (p < 0.0001).
发现MCP1水平较低,与基于CKD进展的预期相反.
观察到n-6/n-3PUFA比率下降 (p = 0.042),这是由增加的n-3脂肪酸驱动的.
在CKD4期FGF23和n-6/n-3比率之间发现了负相关性 (r2 -0.3,p = 0.043),但与MCP1.1没有相关性.

结论:

不同的生物机制可能控制CKD与KTx患者的FGF23,PUFA和MCP1关系.
观察到的差异可能与KTx患者的免疫抑制状态有关.
需要进一步的研究来阐明这些复杂的相互作用.

关键词:

纤维细胞生长因子 23 23 移植脏的情况.单细胞化疗吸引蛋白质 1 1 多不和脂肪酸多不和脂肪酸

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