MYCT1-IFITM2/3 interaction links endothelial endolysosomal trafficking to white adipose tissue expansion - PubMed
5 hours ago
- #obesity
- #endothelial cells
- #metabolic regulation
- MYCT1 is identified as a conserved, pan-endothelial protein essential for white adipose tissue (WAT) expansion.
- Endothelial-specific MYCT1 deletion limits WAT expansion without affecting angiogenesis, adipogenesis, or systemic metabolic parameters.
- MYCT1 interacts with IFITM2/3 to regulate nutrient consumption by the vascular barrier.
- Loss of MYCT1 leads to IFITM2/3 accumulation in early endosomes, causing excessive endolysosomal degradation and mTORC1 hyperactivation.
- Endothelial-specific mTORC1 activation via TSC1 deletion mimics the fat storage defects seen with MYCT1 deficiency.
- The MYCT1-IFITM2/3 complex acts as an endothelial metabolic checkpoint for systemic energy storage.
- Targeting MYCT1-IFITM2/3 could provide new therapeutic avenues for obesity and metabolic disorders.