ArticleAtherosclerosis2014
Genetic manipulation of the ApoF/Stat2 locus supports an important role for type I interferon signaling in atherosclerosis.
Article in Atherosclerosis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Multi-omics analysis reveals novel causal pathways in psoriasis pathogenesis.Journal of translational medicine · 2025Article
- USP18 Curbs the Progression of Metabolic Hypertension by Suppressing JAK/STAT Pathway.Cardiovascular toxicology · 2024Article
- Use of Machine Learning for the Identification and Validation of Immunogenic Cell Death Biomarkers and Immunophenotypes in Coronary Artery Disease.Journal of inflammation research · 2024Article
- A pro-inflammatory and fibrous cap thinning transcriptome profile accompanies carotid plaque rupture leading to stroke.Scientific reports · 2022Article
- Differentiation between thyroid-associated orbitopathy and Graves' disease by iTRAQ-based quantitative proteomic analysis.FEBS open bio · 2021Article
- Article
- ApoF knockdown increases cholesteryl ester transfer to LDL and impairs cholesterol clearance in fat-fed hamsters.Journal of lipid research · 2019Article
- Genetic architecture and adaptations of Nunavik Inuit.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Glycoproteomic Profiling Provides Candidate Myocardial Infarction Predictors of Later Progression to Heart Failure.ACS omega · 2019Article
- Targeted inhibition of STAT3 as a potential treatment strategy for atherosclerosis.Theranostics · 2019Review
- Somatic Editing of Ldlr With Adeno-Associated Viral-CRISPR Is an Efficient Tool for Atherosclerosis Research.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Interferon-α adjuvant therapy decreases the recurrence of early clear cell renal cell carcinoma and improves the prognosis of Chinese patients.Oncotarget · 2017Article
- Review
- Somatic genome editing with CRISPR/Cas9 generates and corrects a metabolic disease.Scientific reports · 2017Article
- Targeted inhibition of STATs and IRFs as a potential treatment strategy in cardiovascular disease.Oncotarget · 2016Review
- HDL proteome remodeling associates with COVID-19 severity.Journal of clinical lipidologyArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Apolipoprotein F (ApoF) is a sialoglycoprotein that is a component of the HDL and LDL fractions of human serum. We sought to test the hypothesis that ApoF plays an important role in atherosclerosis in mice by modulating lipoprotein function. Atherosclerosis was assessed in male low density lipoprotein receptor knockout (Ldlr KO) and ApoF/Ldlr double knockout (DKO) mice fed a Western diet for 16 weeks. ApoF/Ldlr DKO mice showed a 39% reduction in lesional area by en face analysis of aortas (p < 0.05), despite no significant differences in plasma lipid parameters. ApoF KO mice had reduced expression of Interferon alpha (IFNα) responsive genes in liver and spleen, as well as impaired macrophage activation. Interferon alpha induced gene 27 like 2a (Ifi27l2a), Oligoadenylate synthetases 2 and 3 (Oas2 and Oas3) were significantly reduced in the ApoF KO mice relative to wild type controls. These effects were attributable to hypomorphic expression of Stat2 in the ApoF KO mice, a critical gene in the Type I IFN pathway that is situated just 425 base pairs downstream of ApoF. These studies implicate STAT2 as a potentially important player in atherosclerosis, and support the growing evidence that the Type I IFN pathway may contribute to this complex disease.
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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.