Tecr, or trans-2-enoyl-CoA reductase, is an enzyme involved in very-long-chain fatty acid synthesis. It functions in the fourth step of the fatty acid elongation cycle and the sphingosine degradation pathway, playing a crucial role in lipid metabolism [3,4].

In cerebrovascular endothelial cells, EC-specific knockout of Tecr compromises angiogenesis and increases vascular permeability with high levels of transcytosis from neonatal to adult stages, while maintaining vascular tight junctions. Lipidomic analysis shows that Tecr expression is associated with omega-3 fatty acids, which suppress caveolae vesicles formation, suggesting its role in maintaining blood-brain barrier homeostasis [1]. Also, in some studies, homozygous TECR variants in individuals of Hutterite ancestry are associated with intellectual disability, expanding the phenotypic spectrum to include dolicocephaly and dysgenesis of the corpus callosum [2].

In conclusion, Tecr is essential for lipid metabolism-related biological processes. Studies using gene knockout models, especially in the context of blood-brain barrier function and certain genetic intellectual disability phenotypes, have revealed its significance in maintaining physiological functions and its potential as a therapeutic target in central nervous system diseases associated with blood-brain barrier dysfunction [1,2].