Objectives Superficial erosion of coronary plaques due to endothelial loss causes acute coronary syndromes (ACS).Hypochlorous acid (HOCl), a macrophages product can induce endothelial apoptosis.Disturbing (ER) function results in ER stress and unfolded protein response, which tends to restore ER homeostasis but switches to apoptosis when ER stress is prolonged.Therefore, we aimed to investigate whether prolonged ER stress is induced by exogenous HOCl and its underling mechanisms.