During glomerular disease progression, NF-κB activation triggers an inflammatory cascade that produces inflammatory factors, such as IL-10 and MCP-1.Studies have found (186) that TGF-β/SMAD and NF-κB signaling pathways play an important role in HTN, and SMAD7, as a downstream inhibitor of these two pathways, can inhibit proteinuria and serum creatinine, and improve glomerular filtration rate, thereby alleviating the condition of HTN. Here, NFKB1 is linked to hypertensive disorder.