ArticleAnnals of translational medicine2023
TRIM59 attenuates ox-LDL-induced endothelial cell inflammation, apoptosis, and monocyte adhesion through AnxA2.
Article in Annals of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- Effects of evolocumab combined with statin therapy on blood lipids, inflammatory factors, and endothelial function in patients with coronary heart disease.BMC cardiovascular disorders · 2026Article
- lncRNA SND1-IT1/miR-494-3p regulation in ox-LDL-induced endothelial cell injury: novel insights into coronary heart disease pathogenesis and diagnostic biomarkers.European journal of medical research · 2026Article
- IGFBP7 mediates oxLDL-induced human vascular endothelial cell injury by suppressing the expression of SIRT1.Heliyon · 2024Article
- Serum from COVID-19 patients promotes endothelial cell dysfunction through protease-activated receptor 2.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atherosclerosis (AS), a chronic inflammatory vascular disease, is a cause of heart attack and ischemic stroke. Tripartite motif-containing protein 59 (TRIM59), a member of the tripartite motif family, has been reported to be involved in inflammatory diseases. This study was to investigate the role of TRIM59 in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cells and examine the mechanism of TRIM59. Methods: To simulate a cellular model of AS Results: This study showed that TRIM59 expression was decreased in the ox-LDL-induced HUVECs while LOX-1 expression was increased. After transfection with Ov-TRIM59, TRIM59 in ox-LDL-induced HUVECs was increased, and TRIM59 overexpression alleviated the viability damage, inflammation, and apoptosis of the ox-LDL-induced HUVECs. In addition, THP-1 adhesion to the ox-LDL-induced HUVECs was also suppressed by TRIM59 overexpression. This study also showed that TRIM59 could bind to AnxA2 and promote AnxA2 expression in ox-LDL-stimulated HUVECs. Moreover, the rescue experiments revealed that TRIM59 suppressed the viability damage, inflammation, apoptosis, and monocyte adhesion of the ox-LDL-induced HUVECs via AnxA2. Conclusions: TRIM59 protected against ox-LDL-induced AS by binding to AnxA2.
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