ArticleOpen life sciences2024
Knockdown of USP7 alleviates atherosclerosis in ApoE-deficient mice by regulating EZH2 expression.
Article in Open life sciences, 2024. 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.
- Post‑translational modifications in atherosclerosis: Roles, mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2026Review
- Overexpression of miR-7641 activates ox-LDL-induced autophagy in macrophages by regulating USP7.Molecular biology reports · 2026Article
- Ubiquitin-Specific Protease 2 (USP2) as a Modulator of Energy Metabolism: A Review of Studies Using Animal and Cellular Models.Biomedicines · 2026Review
- USP7 Drives Atherosclerosis by Promoting Ferroptosis in Vascular Endothelial Cells via the KIAA1429/NEAT1/CTCF Axis.Biological procedures online · 2026Article
- USP7 Stabilizes USF1 to Aggravate ox-LDL-Induced Endothelial Injury Through the MYD88/NF-κB Pathway in Atherosclerosis.Applied biochemistry and biotechnology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
Atherosclerosis (AS) is a chronic vascular disease associated with lipid accumulation. Understanding the molecular mechanisms of AS is essential. Ubiquitin-specific protease 7 (USP7) is a deubiquitination enzyme involved in various cellular processes, including lipid metabolism. In this study, we aimed to elucidate the role of USP7 in AS progression and its underlying mechanism using ApoE-deficient mice. We found that USP7 ablation improved the morphological characteristics of AS in these mice. USP7 knockdown reduced inflammation, evidenced by decreases in inflammatory markers IL-6, TNF-α, and IL-1β by 35, 40, and 38%, respectively (
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