ArticleJournal of atherosclerosis and thrombosis2024
JNK Pathway-Associated Phosphatase Deficiency Facilitates Atherosclerotic Progression by Inducing T-Helper 1 and 17 Polarization and Inflammation in an ERK- and NF-κB Pathway-Dependent Manner.
Article in Journal of atherosclerosis and thrombosis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- DUSP family phosphatases in cell signaling, inflammation, and chronic diseases.Journal of biomedical science · 2026Review
- The dual-specificity phosphatase JSP1 regulates neutrophil adhesion via integrin-SRC signaling in vascular inflammation.The Journal of biological chemistry · 2026Article
- Insights from GWAS, TWAS, and DEG analysis: CDKN2B-AS1, MAP3K4, and P2RX2-encoded P2X2 receptor identified as potential therapeutic targets for ischemic heart disease in Russian adults and long-living individuals.Frontiers in cardiovascular medicine · 2026Article
- Integrative analysis of programmed cell death pathways reveals prognostic biomarkers and immune infiltration signatures in coronary artery disease.Journal of thoracic disease · 2025Article
- BMSC exosomes deliver JKAP to restore Th17/Treg balance via AKT/ERK, alleviating rheumatoid arthritis.iScience · 2025Article
- The critical role of Th17 cells and IL-17A in autoimmune and inflammation-associated neurological diseases: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Serum JKAP as a potential prognostic biomarker in acute coronary syndrome patients undergoing percutaneous coronary intervention.Frontiers in cardiovascular medicine · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimJNK pathway-associated phosphatase (JKAP) regulates T cell-mediated immunity and inflammation, which are involved in atherosclerosis pathogenesis. This study investigated the effects of JKAP on T-helper (Th) cell polarization, inflammation, and atherosclerotic progression.
methodsSerum JKAP levels were measured in 30 patients with coronary heart disease (CHD) and 30 controls. CHD blood naïve CD4
resultsJKAP was reduced and negatively correlated with the Gensini score, CRP, Th1 cells, Th17 cells, and proinflammatory cytokines in patients with CHD. In vitro, JKAP overexpression suppressed Th1 and Th17 cell differentiation and proinflammatory cytokines, whereas JKAP knockdown exerted the opposite effect; however, JKAP modification did not affect Th2 cell differentiation. Interestingly, JKAP negatively regulated the ERK and NF-κB pathways; meanwhile, the PD98059 and BAY-11-7082 treatments repressed Th1 and Th17 cell differentiation, and attenuated the effect of JKAP knockdown on these indices. In vivo, conditional CD4
conclusionJKAP ablation facilitates atherosclerosis progression by promoting Th1 and 17 polarization and inflammation through regulation of the ERK and NF-κB pathways.
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Registered trials
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