{"id":"858ef673a8a1","type":"article","url":"https://hartvaat.nl/2025/12/18/trim31-in-macrofagen-remt-atherosclerotische-plaquevorming-via-lox-1-afbraak/","title":"TRIM31 in macrofagen remt atherosclerotische plaquevorming via LOX-1-afbraak","title_en":"Macrophage-Specific E3 Ubiquitin Ligase TRIM31 Reduces Atherosclerotic Plaque Formation by Targeting LOX-1","category":"cholesterol","category_label":"Cholesterol","professions":["cardioloog"],"tags":["atherosclerose","ezetimibe","pcsk9-remmers","pelacarsen","plaquekarakterisatie"],"journal":"Circulation","doi":"https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.076514","source_url":"https://doi.org/https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.076514","authors":["Jie Zhang"],"significance":5,"published":"2025-12-18","source_date":"2025-12-18","image":"","kennis":["https://hartvaat.nl/kennis/lipiden/atherosclerose-pathofysiologie/","https://hartvaat.nl/kennis/lipiden/ldl-cholesterol-mechanisme/"],"congress":"","summary_en":"This Circulation study reveals that the macrophage-specific E3 ubiquitin ligase TRIM31 protects against atherosclerosis by targeting LOX-1 for proteasomal degradation. TRIM31 deficiency increases oxidised LDL uptake and foam cell formation, identifying a potential therapeutic target.","created":"2026-07-03T10:25:06Z","updated":"2026-07-03T13:24:33Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Dit onderzoek in Circulation onthult dat het E3 ubiquitine-ligase TRIM31 in macrofagen beschermt tegen atherosclerose door LOX-1 af te breken. Bij TRIM31-deficiëntie neemt de opname van geoxideerd LDL en schuimcelvorming toe. TRIM31 zou een nieuw therapeutisch doelwit kunnen zijn voor de bestrijding van atherosclerose.","abstract_original":"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"}