In summary, our results clarify for the first time that HIF1A-AS2, as a ceRNA for miR-33b, inhibits SMCs proliferation and migration, and facilitates phenotypic switch through regulating HMGA2, which provides a new insight into the molecular mechanism of HIF1A-AS2 in the development of AD, and shed light on a potential target for the treatment of AD. This evidence concerns the gene HMGA2 and Alzheimer disease.