Mitochondrial fission-mediated podocyte dysfunction via CaMKII/Drp1 signaling pathways contributes to lenvatinib-induced renal injury.
Findings provide the first evidence suggesting that increased mitochondrial fission via CaMKII/Drp1 signaling pathways in podocytes contributes to lenvatinib-induced kidney injury, and identify metformin as a clinically viable treatment option for lenvatinib-induced renal injury.