ACTA1 and liver dysplastic nodule: Additionally, HUC-MSCs inhibited the levels of inflammatory factors IL-6, IL-1β, tumour necrosis factor-alpha (TNF-α), TGF-β, MCP-1, and nuclear factor-κB (NF-κB) and downregulated the expression of fibronectin alpha-smooth muscle actin (α-SMA) and collagen IV, suggesting that HUC-MSCs benefit podocytes under high glucose (HG) by suppressing inflammation and fibrosis while delaying the progression of DN 95-97.