Table 4.
Clinical medications of MCs in DKD
| Mediators or Agents | Mechanisms | Effects | Reference(s) |
|---|---|---|---|
| Metformin | Activating AMPK/SIRT1-FoxO1 pathway; stimulating GLP-1R expression |
Enhancing autophagy and slowed down abnormal cell proliferation in high glucose cultured RMCs | 179, 180 |
| Liraglutide | Activating the ERK‑Yap signaling pathway and upregulating Sirt3 expression | Contributing to the shielding of MCs from hyperglycaemia-mediated mitochondrial apoptosis | 183 |
| Liraglutide | Enhancing the Wnt/β-catenin signaling | Suppressing production of extracellular matrix proteins and ameliorating renal injury of diabetic nephropathy | 184 |
| cagliflozin | Inhibiting the PKC/NADPH oxidase pathway | Reducing aberrant ROS production in HG-stimulated MCs and renal mesangial dilatation in db/db mice | 188 |
| Selegiline | Inhibiting TGF-β1/Smad signaling; upregulating heme oxygenase-1 (HO-1) expression |
Alleviating DKD | 190, 191 |
| Enarodustat | Inhibiting the CCL2/MCP-1 production | Reducing proteinuria and glomerular damage | 194 |
| Telmisartan | Reducing AGE-induced MCP-1;governing HG-induced TGFβ1 expression | Alleviating DKD | 195, 196 |