ArticleNature communications2019
CKIP-1 limits foam cell formation and inhibits atherosclerosis by promoting degradation of Oct-1 by REGγ.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 62 citations in OpenAlex.
- A hierarchical theranostic nanoagent for multimodal imaging and targeted foam cell intervention in atherosclerosis.Nature communications · 2026Article
- Smart controlled-release delivery ofRSC advances · 2025Article
- ROS-Responsive Cinnamaldehyde Polymer Nanoparticles Loaded with Puerarin for the Treatment of Atherosclerosis.ACS omega · 2025Article
- Distinct effects of glucocorticoid on pseudorabies virus infection in neuron-like and epithelial cells.Journal of virology · 2025Article
- Dissecting and validation the biomarker of heart failure progression in patients with atherosclerosis by single-cell sequencing, bioinformatics, and machine learning.Frontiers in genetics · 2025Article
- CKIP-1 silencing suppresses OSCC via mitochondrial homeostasis-associated TFAM/cGAS-STING signalling axis.Journal of cellular and molecular medicine · 2024Article
- Bacillus amyloliquefaciens Protect Against Atherosclerosis Through Alleviating Foam Cell Formation and Macrophage Polarization.Current microbiology · 2024Article
- The exoprotein Gbp of Fusobacterium nucleatum promotes THP-1 cell lipid deposition by binding to CypA and activating PI3K-AKT/MAPK/NF-κB pathways.Journal of advanced research · 2024Article
- Associations of CKIP-1 and LOX-1 polymorphisms with the risk of type 2 diabetes mellitus with hypertension among Chinese adults.Acta diabetologica · 2024Article
- Structure, Function, and Allosteric Regulation of the 20S Proteasome by the 11S/PA28 Family of Proteasome Activators.Biomolecules · 2023Review
- Transaldolase inhibits CD36 expression by modulating glutathione-p38 signaling, exerting protective effects against macrophage foam cell formation.Acta biochimica et biophysica Sinica · 2023Article
- CKIP-1 mediatesJournal of oral microbiology · 2023Article
- Identification of a BRAF/PA28γ/MEK1 signaling axis and its role in epithelial-mesenchymal transition in oral submucous fibrosis.Cell death & disease · 2022Article
- Regulation of Life & Death by REGγ.Cells · 2022Review
- Identification of HMOX1 as a Critical Ferroptosis-Related Gene in Atherosclerosis.Frontiers in cardiovascular medicine · 2022Article
- Foam Cells in Atherosclerosis: Novel Insights Into Its Origins, Consequences, and Molecular Mechanisms.Frontiers in cardiovascular medicine · 2022Review
- The Intriguing Role of TLR Accessory Molecules in Cardiovascular Health and Disease.Frontiers in cardiovascular medicine · 2022Review
- PA28γ: New Insights on an Ancient Proteasome Activator.Biomolecules · 2021Review
- Toll-Like Receptor 4 Mediated Oxidized Low-Density Lipoprotein-Induced Foam Cell Formation in Vascular Smooth Muscle Cells via Src and Sirt1/3 Pathway.Mediators of inflammation · 2021Article
- Casein Kinase-2 Interacting Protein-1 Regulates Physiological Cardiac HypertrophyFrontiers in physiology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis-related cardiovascular diseases are the leading cause of mortality worldwide. Macrophages uptake modified lipoproteins and transform into foam cells, triggering an inflammatory response and thereby promoting plaque formation. Here we show that casein kinase 2-interacting protein-1 (CKIP-1) is a suppressor of foam cell formation and atherosclerosis. Ckip-1 deficiency in mice leads to increased lipoprotein uptake and foam cell formation, indicating a protective role of CKIP-1 in this process. Ablation of Ckip-1 specifically upregulates the transcription of scavenger receptor LOX-1, but not that of CD36 and SR-A. Mechanistically, CKIP-1 interacts with the proteasome activator REGγ and targets the transcriptional factor Oct-1 for degradation, thereby suppressing the transcription of LOX-1 by Oct-1. Moreover, Ckip-1-deficient mice undergo accelerated atherosclerosis, and bone marrow transplantation reveals that Ckip-1 deficiency in hematopoietic cells is sufficient to increase atherosclerotic plaque formation. Therefore, CKIP-1 plays an essential anti-atherosclerotic role through regulation of foam cell formation and cholesterol metabolism.
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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.