Abstract: Objective: Dendritic cells (DCs), as important inflammatory cells, are involved in atherosclerosis. Exosomes secreted by DCs (DEXs) have raised abundant attention recently while little is known on the role in dyslipidemia post myocardial infarction. SREBP is an important transcription factor that involves in the lipogenesis through mTOR-SREBP signaling. The pathway inside hepatocytes could be altered by inflammatory signals. We hypothesized that DEXs post myocardial infarction alter lipid metabolism through the mTOR-SREBP pathway. Methods: DCs from mice were stimulated with the supernatants of normal cardiomyocytes (Control-DEX group), or necrotic cardiomyocytes (MI-DEX group). The hepatocytes were treated with the DEXs secreted from the two groups, and the synthesis and secretion of lipids were determined by the enzyme-labeling measuring instrument. The lipid profiles were detected in cell medium. The expression of mTOR-SREBP pathway was measured by Western Blot and RT-PCR. Results: After the intervention of MI-DEX，the level of cholesterol and LDL-c of hepatocytes were enhanced significantly and the expression of mTOR-SREBP increased. With SREBP inhibitor, the functions of synthesis and secretion of lipids declined with decreased expression of mTOR-SREBP. Conclusion: Exosomes derived from dendritic cells may play an important role in the dyslipidemia after myocardial infarction by disturbing mTOR-SREBP pathway in the hepatocytes.