The article "Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice" explores the role of adipose triglyceride lipase (ATGL) in endothelial lipid metabolism and its impact on atherosclerosis. Researchers found that deleting ATGL in endothelial cells leads to neutral lipid accumulation, impairing endothelial function and promoting atherosclerosis. Mechanistically, ATGL loss induces endoplasmic reticulum (ER) stress and inflammation, which heightens proinflammatory signaling. These findings were validated using in vitro and in vivo experiments, including RNA sequencing and functional assays. The study demonstrates that dynamic lipid metabolism in endothelial cells is crucial for maintaining vascular homeostasis and preventing atherosclerosis. The loss of ATGL disrupts this balance, leading to endothelial dysfunction and accelerated atherosclerosis. The research highlights the importance of ATGL in regulating lipid flux through lipid droplets (LDs) and its role in maintaining endothelial function during both normal physiology and chronic disease states. The study provides insights into the molecular mechanisms underlying endothelial dysfunction and atherosclerosis, emphasizing the need for further investigation into the therapeutic potential of targeting ATGL in cardiovascular disease.The article "Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice" explores the role of adipose triglyceride lipase (ATGL) in endothelial lipid metabolism and its impact on atherosclerosis. Researchers found that deleting ATGL in endothelial cells leads to neutral lipid accumulation, impairing endothelial function and promoting atherosclerosis. Mechanistically, ATGL loss induces endoplasmic reticulum (ER) stress and inflammation, which heightens proinflammatory signaling. These findings were validated using in vitro and in vivo experiments, including RNA sequencing and functional assays. The study demonstrates that dynamic lipid metabolism in endothelial cells is crucial for maintaining vascular homeostasis and preventing atherosclerosis. The loss of ATGL disrupts this balance, leading to endothelial dysfunction and accelerated atherosclerosis. The research highlights the importance of ATGL in regulating lipid flux through lipid droplets (LDs) and its role in maintaining endothelial function during both normal physiology and chronic disease states. The study provides insights into the molecular mechanisms underlying endothelial dysfunction and atherosclerosis, emphasizing the need for further investigation into the therapeutic potential of targeting ATGL in cardiovascular disease.