We scrutinized our GSEA data to explore whether Trf1 deletion in fibroblasts contributes to injury-induced endothelial dysfunction in kidney fibrosis and observed a significant reduction in angiogenesis (NES: 1.77), marked by the downregulation of Pecam1 and Kdr mRNA levels, and an increase in hypoxia (NES: 1.54), accompanied by elevated mRNA levels of Hif1-α and CA9, in Trf1flox/flox mice compared with Trf1 mice (Fig. 5a–c). This evidence concerns the gene HIF1A and endothelial dysfunction.