The balance between proliferation and apoptosis of vascular smooth muscle cells (VSMCs) plays a critical role in the initiation of atherosclerosis. LncRNA-MEG3 is involved in the pathophysiology of atherosclerosis through regulation of endothelial cell proliferation and migration. Its effect on the dysfunction of VSMCs and the corresponding mechanisms are actively researched. In this study, we observed that downregulated lneRNA-MEG3 expression was inversely correlated with the microRNA-26a level in coronary artery disease tissues. The overexpression of lneRNA-MEG3 could inhibit VSMCs proliferation while facilitating apoptosis. Moreover, alteration in the miR-26a/Smad1 axis could antagonize this effect. Bioinformatic analysis indicated that IncRNA-MEG3 could interact with miR-26a via complementary binding sites. The enforced expression of IncRNA-MEG3 could reduce the level of miR-26a in VSMCs, while the expression of Smad1 increases. Further, the direct binding between IncRNA-MEG3 and miR-26a was confirmed via dual-luciferase reporter assay, which indicated that lnc-MEG3 could sponge miR-26a as a competing endogenous RNA. In summary, we propose that lncRNA-MEG3 modulates the proliferation/apoptosis balance of VSMCs in atherosclerosis by regulating the miR-26a/Smad1 axis.