AIM:To investigate the role of phosphoenolpyruvate carboxykinase 1(PCK1)in the proliferation and migration of mouse vascular smooth muscle cells(VSMCs)and the underlying mechanism.METHODS:The prolif-eration and migration of mouse VSMCs were induced by platelet-derived growth factor(PDGF)-BB.The cells were divided into a vehicle group and a PDGF-BB group.The expression of PCK1 was detected by Western blot and immunofluores-cence staining.The mouse Pck1 siRNA(si Pck1)were transfected into mouse VSMCs to silence PCK1.The cells were di-vided into the vehicle,si Pck1+vehicle,PDGF-BB and si Pck1+PDGF-BB groups.The protein level of PCK1 was detected by Western blot.The proliferation was explored by Ki-67 immunofluorescence staining and the viability was detected by CCK-8 assay.The migration was determined by a scratch test.Mitochondrial dynamics were observed via transmission electron microscopy.A lentivirus carrying dynamin-related protein 1(Drp1)gene(lenti-Drp1)was transfected into VSMCs to induce them to overexpress DRP1.The cells were divided into the PDGF-BB,si Pck1+PDGF-BB,lenti-Drp1+PDGF-BB and lenti-Drp1+si Pck1+PDGF-BB groups.Proliferation,migration and mitochondrial dynamics were measured as described above.RESULTS:PDGF-BB increased the protein expression of PCK1 and DRP1,cell viability,the per-centage of Ki-67-positive cells,the wound healing rate and mitochondrial division in VSMCs.These effects were sup-pressed when PCK1 protein expression was silenced.After DRP1 was overexpressed,the inhibitory effects of PCK1 silenc-ing on cell viability,the percentage of Ki-67-positive cells,the wound healing rate and mitochondrial division were signifi-cantly reversed.CONCLUSION:PCK1 promotes the mitochondrial division,proliferation and migration of VSMCs in mice by upregulating the expression of DRP1.