ArticleThe Journal of clinical investigation2022
Disruption of USP9X in macrophages promotes foam cell formation and atherosclerosis.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 119 citations in OpenAlex.
- New insights into the ACLY-mediated metabolic and epigenetic interplay in macrophages.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Sex Differences and Oxidative Stress in Cardiovascular Disease.Physiology (Bethesda, Md.) · 2026Review
- ACT001 suppresses ox-LDL-mediated macrophage ferroptosis via activating the NRF2 pathway: AnExperimental and therapeutic medicine · 2026Article
- The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII-δ.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Deubiquitinases as Regulators and Therapeutic Targets in Vascular Diseases.International journal of molecular sciences · 2026Review
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Macrophage membrane-functionalized biomimetic Yiqi Huoxue formula nanoparticles improve atherosclerosis by regulating smooth muscle cell phenotypic transition via the KLF4/NF-κB pathway.Chinese medicine · 2026Article
- Macrophage USP9X attenuates colitis by restricting oncostatin M production via K27-linked deubiquitination of STAT1.Cellular & molecular immunology · 2026Article
- RNF2 mediates H2A ubiquitination to promote colitis via suppressing monocyte-macrophage transition in mice.Nature communications · 2026Article
- Dapagliflozin binds PRMT7 to inhibit p38 MAPK phosphorylation and macrophage foam cell formation in atherosclerosis.iScience · 2026Article
- Visualization analysis of research hotspots and trends in Type B Aortic Dissection based on bibliometrics.Journal of cardiothoracic surgery · 2026Review
- USP25 in atherosclerosis: a new kid on the block.EBioMedicine · 2026Article
- GFPT2 promotes macrophage dysfunction in atherosclerosis via ACADL glycosylation-dependent suppression of ACADL and Arg1.Cellular and molecular life sciences : CMLS · 2026Article
- USP25 regulates atherosclerosis by restricting RIPK1-mediated inflammatory responses.EBioMedicine · 2026Article
- Chaperone-Mediated Autophagic Degradation of USP9X in Macrophages Exacerbates Postmyocardial Infarction Inflammation and Cardiac Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage FTO deficiency accelerates atherosclerosis via PACS2-mediated activation of the PPARγ lipid signaling pathway.Journal of translational medicine · 2026Article
- Nanocomposite LL37-gold nanoparticles with puerarin for periodontitis-linked atherosclerosis.Journal of nanobiotechnology · 2026Article
- Joint association of systemic inflammatory response index and thromboelastography maximum amplitude with the risk of early atherosclerosis in patients with rheumatoid arthritis.Clinical and experimental medicine · 2026Article
- Resibufogenin protects against atherosclerosis in ApoEJournal of advanced research · 2026Article
- Natural Products Modulate Plaque Macrophage Functional Programs in Atherosclerosis.Drug design, development and therapy · 2026Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subendothelial macrophage internalization of modified lipids and foam cell formation are hallmarks of atherosclerosis. Deubiquitinating enzymes (DUBs) are involved in various cellular activities; however, their role in foam cell formation is not fully understood. Here, using a loss-of-function lipid accumulation screening, we identified ubiquitin-specific peptidase 9 X-linked (USP9X) as a factor that suppressed lipid uptake in macrophages. We found that USP9X expression in lesional macrophages was reduced during atherosclerosis development in both humans and rodents. Atherosclerotic lesions from macrophage USP9X-deficient mice showed increased macrophage infiltration, lipid deposition, and necrotic core content than control apolipoprotein E-KO (Apoe-/-) mice. Additionally, loss-of-function USP9X exacerbated lipid uptake, foam cell formation, and inflammatory responses in macrophages. Mechanistically, the class A1 scavenger receptor (SR-A1) was identified as a USP9X substrate that removed the K63 polyubiquitin chain at the K27 site. Genetic or pharmacological inhibition of USP9X increased SR-A1 cell surface internalization after binding of oxidized LDL (ox-LDL). The K27R mutation of SR-A1 dramatically attenuated basal and USP9X knockdown-induced ox-LDL uptake. Moreover, blocking binding of USP9X to SR-A1 with a cell-penetrating peptide exacerbated foam cell formation and atherosclerosis. In this study, we identified macrophage USP9X as a beneficial regulator of atherosclerosis and revealed the specific mechanisms for the development of potential therapeutic strategies for atherosclerosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.