ArticleClinical and translational medicine2025
Annexin A8 deficiency delays atherosclerosis progression.
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Conditional knockout of membrane-type I matrix metalloproteinase in smooth muscle cells of adult mice alleviates atherosclerosis without affecting basic cardiovascular function.Clinical and translational medicine · 2026Article
- Chitinase-like proteins de-N-glycosylating CD36 modify cholesterol metabolism in atherosclerotic macrophages.Nature communications · 2026Article
- Human papillomavirus E7 inhibits immune responses in keratinocytes by activating HTRA1‑mediated mitophagy.International journal of molecular medicine · 2026Article
- Annexin A8 deficiency delays atherosclerosis progression.Clinical and translational medicine · 2025Article
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Authors and funding
15 authors.
Funding
Abstract
backgroundAtherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids and leukocytes within the arterial wall. By studying the aortic transcriptome of atherosclerosis-prone apolipoprotein E (ApoE
methodsRNA-Seq analysis was performed on aortas from ApoE
resultsRNA-Seq unveiled AnxA8 as one of the most significantly upregulated genes in atherosclerotic aortas of ApoE
conclusionOur findings demonstrate that AnxA8 promotes the progression of atherosclerosis by modulating endothelial-leukocyte interactions. Interventions capable of reducing AnxA8 expression in endothelial cells may delay atherosclerotic plaque progression. KEY POINTS: This study shows that AnxA8 is upregulated in aorta of atheroprone mice and in human atherosclerotic plaques. Germline AnxA8 deficiency reduces platelet and leukocyte recruitment to activated endothelium as well as atherosclerotic burden, plaque size, and macrophage accumulation in mice. AnxA8 regulates oxLDL-induced adhesion molecules expression in aortic endothelial cells. Our data strongly suggest that AnxA8 promotes disease progression through regulation of adhesion and influx of immune cells to the intima. Endothelial specific silencing of AnxA8 reduced atherosclerosis progression. Therapeutic interventions to reduce AnxA8 expression may delay atherosclerosis progression.
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