Ceramide C16:0, a key metabolite in sphingolipid metabolism, has been found to play a critical role in the pathogenesis of atherosclerosis. This comprehensive review elucidates the pathogenic mechanism by which ceramide C16:0 contributes to the development of atherosclerosis, including activating inflammatory responses, inducing insulin resistance, impairing endothelial function, disrupting mitochondrial homeostasis, and exacerbating endoplasmic reticulum stress. Clinical evidence demonstrates that the elevated levels of plasma ceramide C16:0 exhibit a strong correlation with an increased risk of cardiovascular events, supporting its potential utility as an independent prognostic biomarker. Inhibition of ceramide C16:0 synthesis or blockade of its receptors demonstrates promising therapeutic potential. Future research should focus on developing specific inhibitors, refining cardiovascular risk assessment models, and exploring integrative treatment strategies, aiming to offer new strategies for preventing and treating atherosclerosis.
Chen et al. (Wed,) studied this question.