Circadian clocks are timekeeping mechanisms that allow organisms to anticipate daily changes and efficiently maintain temporal coordination of physiological processes in a rhythmic environment. Chronic desynchronization between the internal circadian system and environmental cues has been associated with an increased risk of developing several pathologies, including cardiovascular diseases. The circadian clock machinery has been described in cardiovascular tissues and organs, as well as in the different cell types that conform the vasculature. Among them, smooth muscle cells (SMCs) are the most abundant cell type of the blood vessels and play a key role in arterial remodeling during the development of atherosclerosis. During this process, SMCs migrate to the intima layer of the arterial wall and switch from a contractile to a synthetic phenotype. In the present study, a well-established in vitro porcine model representative of two populations of SMCs was used to characterize the involvement of the circadian clock in the development of atherosclerosis.