Many physiological events in mammals, including locomotor activity, sleep, blood pressure, circulating hormones and energy metabolism, exhibit rhythmic fluctuations over the 24-hour day.Recent studies have indicated that clock genes intensively regulate the homeostasis of cardiovascular system.However, the molecular mechanism through which circadian clock and cardiovascular system are integrated remains unknown.Our study demonstrated that Smarcd1, a member of SWI/SNF chromatin remodeling complex family, showed rhythmic expression pattern in serumshocked vascular smooth muscle cells (VSMCs).Stimulation of free fatty acids (FFAs) reduced the oscillation amplitude of clock gene expression, and inhibited Smarcd1 expression levels.More importantly, overexpression of Smarcd1 partially rescued the reduction of clock gene oscillation induced by FFAs.As to the VSMC physiological homeostasis, we found that overexpression of Smarcd1 significantly inhibited FFAs-induced VSMC proliferation, migration, adhesion and ROS production, as well as ERK/MAPK and Akt phosphorylation levels.In addition, knockdown of Bmal1, a critical regulator in circadian clock, markedly abolished the inhibitory effects of Smarcd1 on VSMCs.At the molecular level, Smarcd1 binds to RORα and synergistically activates the transcriptional activity of Bmal1 promoter.Taken together, Smarcd1 plays an important role in the integration of circadian clock and physiological homeostasis of VSMCs.