Cardiac aging facilitates cardiovascular diseases. For instance, the incidence of atrial fibrillation increases by aging of the population. Elevated lipids level is a major risk factor for cardiovascular diseases, among those very-low-density-lipoprotein (VLDL) which carries major triglyceride, has much limited scientific studies and evidence. Our research team has found that VLDL exhibits lipotoxicity to atrial cells and tissue and causes vulnerability to atrial fibrillation. We hypothesize that cardiac senescence is involved in the mechanisms of VLDL-induced atrial cardiomyopathy. We also found that VLDL has quality change upon the condition of metabolic syndrome. We therefore also hypothesize that VLDL ofMetS can enhance cardiac senescence and accelerate cardiac aging. This project is proposed to elaborate how VLDL affects cardiac senescence-related cellular signaling in cardiac atria. In the current study, we aim to explore the mechanism of VLDL on cardiomyocytes by purifying VLDL of metabolic syndrome patients and treating it toward cardiomyocyte HL-1. The main purpose of our research is to discuss the lipotoxicity of lipoprotein and how it induces the death and aging of cardiomyocytes, especially VLDL.

螢幕快照 2021 10 24 下午11.04.24