Salidroside, a key compound from Rhodiola rosea, exhibits potent pharmacological effects, including antioxidant, anti-inflammatory, and renoprotective properties. It has shown promise in the prevention and treatment of various renal diseases, such as diabetic nephropathy, acute kidney injury, and renal fibrosis. The mechanisms of salidroside involve the regulation of gene and protein expression in renal cells, including TNF-α, TGF-β, IL-1β, IL-17A, IL-6, MCP-1, Bcl-2, VEGF, ECM proteins, caspase-3, HIF-1α, BIM, and modulation of pathways such as AMPK/SIRT1, Nrf2/HO-1, Sirt1/PGC-1α, ROS/Src/Cav-1, Akt/GSK-3β, TXNIP-NLRP3, ERK1/2, TGF-β1/Smad2/3, PI3K/Akt, Wnt1/Wnt3α/β-catenin, TLR4/NF-κB, MAPK, JAK2/STAT3, and SIRT1/Nrf2. These mechanisms contribute to its protective effects against oxidative stress, inflammation, and fibrosis in the kidney. Salidroside has been shown to reduce oxidative stress, inhibit apoptosis, and modulate inflammatory responses in renal cells. It can improve renal function by reducing blood glucose levels, regulating blood lipid, and activating signaling pathways such as AMPK, Nrf2/HO-1, and Akt/GSK-3β. In diabetic nephropathy, salidroside inhibits the progression of kidney damage by reducing oxidative stress, inflammation, and fibrosis. It also protects against renal ischemia-reperfusion injury by reducing oxidative stress, inflammation, and apoptosis in renal cells. In renal fibrosis, salidroside inhibits the expression of TGF-β1, which is a key factor in the progression of fibrosis. It also reduces the expression of fibrosis-related proteins such as TGF-β1, p-Smad2, and p-Smad3, and inhibits the TGF-β1/Smad2/3 pathway, thereby slowing down the pathological changes in kidney tissue. Salidroside also inhibits EMT (epithelial-mesenchymal transition) by reducing the expression of EMT markers and inflammatory factors, and by inhibiting the TLR4/NF-κB and MAPK signaling pathways. Overall, salidroside shows significant potential as a therapeutic agent for the prevention and treatment of various renal diseases, including diabetic nephropathy, acute kidney injury, and renal fibrosis. Its mechanisms of action involve the regulation of multiple signaling pathways and the modulation of inflammatory and fibrotic processes in the kidney.Salidroside, a key compound from Rhodiola rosea, exhibits potent pharmacological effects, including antioxidant, anti-inflammatory, and renoprotective properties. It has shown promise in the prevention and treatment of various renal diseases, such as diabetic nephropathy, acute kidney injury, and renal fibrosis. The mechanisms of salidroside involve the regulation of gene and protein expression in renal cells, including TNF-α, TGF-β, IL-1β, IL-17A, IL-6, MCP-1, Bcl-2, VEGF, ECM proteins, caspase-3, HIF-1α, BIM, and modulation of pathways such as AMPK/SIRT1, Nrf2/HO-1, Sirt1/PGC-1α, ROS/Src/Cav-1, Akt/GSK-3β, TXNIP-NLRP3, ERK1/2, TGF-β1/Smad2/3, PI3K/Akt, Wnt1/Wnt3α/β-catenin, TLR4/NF-κB, MAPK, JAK2/STAT3, and SIRT1/Nrf2. These mechanisms contribute to its protective effects against oxidative stress, inflammation, and fibrosis in the kidney. Salidroside has been shown to reduce oxidative stress, inhibit apoptosis, and modulate inflammatory responses in renal cells. It can improve renal function by reducing blood glucose levels, regulating blood lipid, and activating signaling pathways such as AMPK, Nrf2/HO-1, and Akt/GSK-3β. In diabetic nephropathy, salidroside inhibits the progression of kidney damage by reducing oxidative stress, inflammation, and fibrosis. It also protects against renal ischemia-reperfusion injury by reducing oxidative stress, inflammation, and apoptosis in renal cells. In renal fibrosis, salidroside inhibits the expression of TGF-β1, which is a key factor in the progression of fibrosis. It also reduces the expression of fibrosis-related proteins such as TGF-β1, p-Smad2, and p-Smad3, and inhibits the TGF-β1/Smad2/3 pathway, thereby slowing down the pathological changes in kidney tissue. Salidroside also inhibits EMT (epithelial-mesenchymal transition) by reducing the expression of EMT markers and inflammatory factors, and by inhibiting the TLR4/NF-κB and MAPK signaling pathways. Overall, salidroside shows significant potential as a therapeutic agent for the prevention and treatment of various renal diseases, including diabetic nephropathy, acute kidney injury, and renal fibrosis. Its mechanisms of action involve the regulation of multiple signaling pathways and the modulation of inflammatory and fibrotic processes in the kidney.