Macrophages play a key role in atherosclerotic plaque formation and rupture. These phagocytic cells are important in the scavenging of modified lipoproteins, unwanted or dead cells and cellular debris through efferocytosis. Sirtuin1 (Sirt1), a member of the conserved sirtuin family and a key regulator in the progression of atherosclerosis exerts protective effects by regulating autophagy, a well‑known survival mechanism. Inhibition of autophagy may also result in defective efferocytosis. This study aimed to investigate the effect of Sirt1 on the efferocytosis of oxidized low-density lipoprotein (ox-LDL)-induced apoptotic RAW264. 7 cells through upregulation of autophagy. The apoptotic cells were incubated with high and low concentrations of Sirt1 activator resveratrol (RSV) and Sirt1 inhibitor nicotinamide (NAM) as well as autophagy inhibitor 3-methyladenine (3-MA)+ low concentration RSV. Apoptosis was determined by flow cytometry (FCM) of annexin-V/propidium iodide (AV/PI) dual staining. Total proteins were extracted and protein levels were detected through western blot analysis. The ox-LDL uptake and efferocytosis of apoptotic RAW264. 7 cells were detected by oil red O staining and calculation of the phagocytic index of apoptotic RAW264. 7 cells. The expression of Sirt1 and autophagy marker proteins was simultaneously increased with the stimulation of low concentration RSV (all P< 0.05) and decreased in low and high NAM groups (all P< 0.05), compared with the control group. Efferocytosis was highest in the low concentration RSV group (P< 0.001) and relatively lower in the low and high concentration NAM groups (both P< 0.05) compared with the control group, which was similar to the change in the expression of Sirt1 and autophagy marker proteins. The results showed that the efferocytosis of apoptotic RAW264. 7 cells was significantly improved with the upregulation of Sirt1‑mediated autophagy. Therefore, Sirt1 may serve as a novel therapeutic target for the treatment of atherosclerosis.