sFlt-1 in Chronic Kidney Disease: Friend or Foe?

被引：7
|
作者：
Matsui, Masaru [1 ,2 ]
Onoue, Kenji [3 ]
Saito, Yoshihiko [4 ]
机构：
[1] Nara Prefecture Gen Med Ctr, Dept Nephrol, 2-897-5 Shichijo Nishimachi, Nara 6308581, Japan
[2] Nara Med Univ, Dept Nephrol, 840 Shijo Cho, Kashihara, Nara 6348521, Japan
[3] Nara Med Univ, Dept Cardiol, 840 Shijo Cho, Kashihara, Nara 6348521, Japan
[4] Nara Prefecture Seiwa Med Ctr, 1-14-16 Mimuro,Sango Cho, Kashihara, Nara 6360802, Japan
来源：
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2022年 / 23卷 / 22期
关键词：
PlGF; sFlt-1; cardiorenal connection; ENDOTHELIAL-GROWTH-FACTOR; TYROSINE KINASE-1; CARDIOVASCULAR EVENTS; FACTOR EXPRESSION; RECEPTOR; VEGF; CONTRIBUTES; ANGIOGENESIS; PROGRESSION; PLAQUES;
D O I：
10.3390/ijms232214187
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Placental growth factor (PlGF) and its receptor, fms-like tyrosine kinase-1 (Flt-1), are important regulators involved in angiogenesis, atherogenesis, and inflammation. This review article focuses on the function of PlGF/Flt-1 signaling and its regulation by soluble Flt-1 (sFlt-1) in chronic kidney disease (CKD). Elevation of circulating sFlt-1 and downregulation of sFlt-1 in the vascular endothelium by uremic toxins and oxidative stress both exacerbate heart failure and atherosclerosis. Circulating sFlt-1 is inconsistent with sFlt-1 synthesis, because levels of matrix-bound sFlt-1 are much higher than those of circulating sFlt-1, as verified by a heparin loading test, and are drastically reduced in CKD.
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页数：13
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