Current consensus suggests that these SGLT2 inhibitors can activate tubuloglomerular feedback to reduce intraglomerular hypertension, alleviate proximal tubular metabolic stress to restore mitochondrial function, and suppress inflammatory and fibrotic pathways such as NLRP3 inflammasome and TGF-β signaling cascades (39, 40). This evidence concerns the gene SLC5A2 and Hypertension.