ApoM, short for apolipoprotein M, is a member of the apolipoprotein family. It is primarily expressed and secreted from the liver and kidneys. ApoM is the main chaperone of sphingosine-1-phosphate (S1P), a small signalling molecule involved in numerous physiologic and pathophysiologic processes. Together, ApoM/S1P plays a role in several biological mechanisms, such as inflammation, endothelial cell permeability, and lipid turnover [1,2].

ApoM-deficient mice display an increased activity in brown adipose tissue and a concomitant fast turnover of triglycerides, indicating that ApoM/S1P axis plays a significant role in maintaining a balanced triglyceride metabolism [4]. In addition, gain-and loss-of-function mouse models implicated the forkhead box O transcription factors (FoxO1,3,4) in the regulation of both ApoM and HDL-associated S1P, which has important implications for potential FoxO-based therapies designed to treat lipid and carbohydrate abnormalities associated with human metabolic disease and CVD [3].

In conclusion, ApoM is crucial for transporting S1P and is involved in multiple biological processes like lipid metabolism, inflammation, and endothelial cell function. Mouse models, especially those with ApoM deficiency, have revealed its role in triglyceride turnover and in metabolic diseases, providing insights into potential therapeutic targets for diseases such as hypertriglyceridemia, metabolic syndrome, and related cardiovascular diseases.