The dysregulation of proliferation and migration of vascular smooth muscle cells (VSMCs) contributes to atherosclerosis (AS) and accumulating reports indicate the crucial roles of long noncoding RNA (lncRNA) in AS. However, the roles of small nucleolar RNA host gene 12 (SNHG12) in regulating the phenotypes of VSMCs and atherosclerosis remain largely unknown. qRT-PCR was used to detect the expression levels of SNHG12 and miR-199a-5p in in vivo AS model and VSMCs treated by oxidized low density lipoprotein (ox-LDL). Proliferation ability, migration ability, and apoptosis of VSMCs were tested by CCK-8, Transwell assay, and TUNEL assay respectively. StarBase database was used to predict the binding sites between miR-199a-5p and SNHG12. Interaction between miR-199a-5p and SNHG12 was validated by qRT-PCR, Western blot, and luciferase reporter assay. Western blot was used to examine the effects of SNHG12 and miR-199a-5p on the expression of hypoxia-inducible factor 1α (HIF-1α). We found that the expression level of SNHG12 was significantly increased in animal model and VSMCs treated by ox-LDL. Knockdown of SNHG12 suppressed the proliferation and migration ability of VSMCs, while overexpression of SNHG12 had opposite effects. Mechanically, we validated that miR-199a-5p was a target of SNHG12, and the target gene of miR-199a-5p, hypoxia inducible factor 1α (HIF-1α) could be indirectly and positively regulated by SNHG12. In conclusion, SHNG12 targeting miR-199a-5p/HIF-1α contributed to the pathophysiological process of AS by regulating the phenotypes of VSMCs, and could be a potential therapy target for this disease. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.