Cardiac aging promotes cardiovascular disease. For example, the incidence of atrial fibrillation increases as the population ages. Elevated blood lipid levels are a major risk factor for cardiovascular disease, with very limited scientific research and evidence on very low-density lipoprotein (VLDL), which carries the major triglyceride. Our research team found that VLDL is lipotoxic to atrial cells and tissues and contributes to a predisposition to atrial fibrillation. We hypothesized that cardiac aging is involved in the mechanism of VLDL-induced atrial cardiomyopathy. We also found that VLDL has mass changes in the context of metabolic syndrome (MetS). Therefore, we also hypothesized that VLDL of MetS could enhance cardiac aging and accelerate cardiac aging. The aim of this project is to illustrate how VLDL affects cellular signaling in the atrium associated with cardiac aging. In the current study, we aimed to explore the mechanism of action of VLDL on cardiomyocytes by purifying VLDL from patients with metabolic syndrome and processing it into cardiomyocyte HL-1. The main aim of our study was to investigate the lipotoxicity of lipoproteins and how it induces death and senescence in cardiomyocytes, especially VLDL.