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Published on: November 10, 2021
sFlt-1 in Chronic Kidney Disease: Friend or Foe?
Masaru Matsui1,2, Kenji Onoue3, Yoshihiko Saito4
1Department of Nephrology, Nara Prefecture General Medical Center, 2-897-5 Shichijo-Nishimachi, Nara 630-8581, Japan.
Abstract:
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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