Aim To explore the effect of growth differentiation factor 11 (GDF11) on macrophage reverse cholesterol transport and uncover the potential mechanism. Methods Mouse peritoneal macrophages were treated with oxidized low density lipoprotein (ox-LDL), GDF11 and activin receptor-like kinase 7 (ALK7) inhibitor SB431542 for 24 hours. The lipid accumulation was observed with oil red O staining, and the mRNA and protein expression levels of GDF11, ABCA1 and ABCG1 were determined by real-time PCR and Western blot. Mice were given intraperitoneal injection of exogenous GDF11. Peritoneal macrophages were labeled with ³H-cholesterol, then the labeled macrophages were injected into mice intraperitoneally. The mice feces were collected every 8 hours and the liver and blood samples of mice were gathered after 48 hours since cell injection. The radioactivity of ³H was detected to measure the reverse cholesterol transport level. Results After treated with ox-LDL for 24 hours, ox-LDL induced the accumulation of lipid in macrophage and inhibited the GDF11 mRNA and protein expression level. GDF11 treatment effectively inhibited the lipid accumulation in macrophage induced by ox-LDL. Exogenous GDF11 effectively induced macrophage ABCA1 mRNA expression and increased the cholesterol reverse transport level in vivo. However, after treated with GDF11 and ALK7 inhibitor SB431542, the inhibitory effect of GDF11 on intracellular lipid accumulation induced by ox-LDL was antagonized, and the upregulation of ABCA1 expression was also inhibited. Conclusion GDF11 regulates the expression of ABCA1 through ALK7, thus promoting the reverse transport of cholesterol in macrophage.