TRIM31 in macrofagen remt atherosclerotische plaquevorming via LOX-1-afbraak

BACKGROUND:Atherosclerosis is a chronic inflammatory disease marked by lipid accumulation and immune cell infiltration in arterial walls. Macrophages contribute by internalizing oxidized low-density lipoprotein, forming foam cells, and driving inflammation. The ubiquitin–proteasome system regulates immune and inflammatory responses in atherosclerosis. This study investigated the protective role of TRIM31 (tripartite motif-containing 31), an E3 ubiquitin ligase, in macrophage lipid metabolism and inflammation through selective regulation of LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1).METHODS:Transcriptomic profiling, macrophage-specificTrim31knockout (Trim31fl/flLyz2cre) and overexpression (Trim31Lyz2-KI) mice, andLox-1knockout (Lox-1−/−) models were used to examine the impact of TRIM31 in vivo (n=8 per group). TRIM31 substrates were identified using single-cell RNA sequencing of atherosclerotic aortas and proteomic/immunoprecipitation–mass spectrometry analyses. Fun