Online Supplementary of Shi et al manuscript June 21 2022.pdf

There are supplemental data and figures of one manuscript titled as VEGFR2 insufficiency enhances phosphotoxicity and undermines Klotho’s protection against peritubular capillary rarefaction and kidney fibrosis. This basic research manuscript is accepted for publication in American Journal of Physiology-Renal Physiology. This research paper studied interplay of type 2 of vascular endothelial growth factor receptor (VEGFR2), high dietary phosphate and Klotho, an anti-aging protein, in peritubular structure and kidney fibrosis. Klotho protein was shown to maintain VEGFR2 expression in the kidney and reduce high phosphate-induced cell injury. But Klotho cytoprotection was attenuated by VEGFR2 inhibition. Thus, normal VEGFR2 function is required for vascular integrity and Klotho to exert vascular protective and anti-fibrotic actions in the kidney.

本研究配套数据与图表来自一篇题为《VEGFR2不足增强磷酸毒性并削弱Klotho对抗肾小管周围毛细血管稀疏与肾纤维化的保护作用》的基础研究手稿。该手稿已被《美国生理学杂志-肾脏生理学》（American Journal of Physiology-Renal Physiology）接收待刊。本研究探讨了2型血管内皮生长因子受体（vascular endothelial growth factor receptor 2, VEGFR2）、高膳食磷与抗衰老蛋白Klotho在肾小管周围结构及肾纤维化中的相互作用。研究表明，Klotho蛋白可维持肾脏内VEGFR2的表达，并减轻高磷诱导的细胞损伤。但VEGFR2抑制会削弱Klotho的细胞保护作用。因此，肾脏要维持血管完整性且使Klotho发挥血管保护与抗纤维化作用，均依赖正常的VEGFR2功能。