Slc44a2, encoding the choline transporter-like protein CTL2, is involved in multiple biological functions. It plays a role in platelet aggregation, neutrophil activation, and is also associated with the regulation of mitochondrial function through choline transport into mitochondria [3,5]. It has been linked to various pathways including those related to thrombosis and vascular-related processes. Genetic models such as knockout mice are valuable for studying its functions.

In aortic aneurysm, VSMC-specific Slc44a2-knockout mice are more susceptible to aortic aneurysm under Ang II infusion, indicating that Slc44a2 is protective. Mechanistically, it interacts with NRP1 and ITGB3 to activate the TGF-β/SMAD signaling pathway, promoting contractile gene expression. Inhibition of Slc44a2 facilitates VSMC phenotypic switching to a synthetic state, contributing to the development of aortic aneurysm [1,2].

In venous thrombosis, Slc44a2-deficient mice have a reduced response in the stenosis-driven venous thrombosis model, suggesting its role in the initiation of venous thrombosis, potentially related to platelet-neutrophil interaction [4].

In conclusion, Slc44a2 is crucial for multiple biological processes. Its functions revealed through gene-knockout mouse models have significant implications in diseases like aortic aneurysm and venous thrombosis, highlighting its potential as a therapeutic target for these vascular-related conditions.