Figure 7.

ACh improved LD lipolysis and PLIN5-mediated LD-mitochondria interaction in PA-induced cardiomyocyte apoptosis. In cultured NRVCs, (i) PA induces an increase in lipid uptake, LD formation and a remarkable reduction in lipolysis, accompanied by impairments in LD-mitochondria interactions and decreased PLIN5 expression, resulting in LD accumulation and mitochondrial dysfunction, which eventually induce cardiomyocyte apoptosis. (ii) ACh normalizes changes in lipid uptake, LD production and LD lipolysis and improves LD-mitochondria associations and PLIN5 expression, thereby reducing the excess deposition of LDs and mitochondrial dysfunction and ultimately suppressing apoptosis of PA-treated NRVCs. (iii) PLIN5 siRNA abolishes the ACh-induced attenuation of LD accumulation, mitochondrial damage, and cardiomyocyte apoptosis. ACh, acetylcholine; ATGL, adipose triglyceride lipase; ATP, adenosine triphosphate; CD36, cluster of differentiation 36; CPT1B, carnitine palmitoyl transferase 1B; DAG, diacylglycerol; FA, fatty acid; HSL, hormone-sensitive lipase; LD, lipid droplet; MAG, monoacylglycerol; MGL, monoacylglycerol lipase; PA, palmitate; PLIN, perilipin; ROS, reactive oxygen species; TAG, triacylglycerol; Ψm, mitochondrial membrane potential