Lysyl-tRNA synthetase 1 promotes atherogenesis via autophagy-related secretion and inflammation.

ABSTRACT: Lysyl-tRNA synthetase 1 (KARS1), an aminoacyl-tRNA synthetase, was recently identified as a secreted pro-inflammatory agent. However, the vascular secretion and functions of KARS1 have not been characterized. This study investigated the secretion mechanisms of KARS1 and explored its functional roles in vascular biology. We found that KARS1 expression was upregulated by oscillatory shear stress, an atherogenic factor, suggesting the presence of free KARS1 dissociated from aminoacyl-tRNA synthetase complexes. Moreover, in the presence of Ca²⁺, serum starvation triggered free cytosolic KARS1 release from endothelial cells via secretory autophagy. Both phosphatidylinositol 3-phosphate kinase and caveolin-1 were either supplementary or essential for KARS1 secretion. Secreted KARS1 co

SUBMITTER: Yun K 

PROVIDER: S-EPMC11961584 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature