ArticleJournal of lipid research2015
Macrophage apoAI protects against dyslipidemia-induced dermatitis and atherosclerosis without affecting HDL.
Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
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
22 citing papers in PubMed, 31 citations in OpenAlex.
- Apolipoprotein A-I mediates function of follicular regulatory T cells and type 2 follicular helper T in allergic rhinitis.The World Allergy Organization journal · 2025Article
- Serum ASGR2 level: an efficacy biomarker for balloon pulmonary angioplasty in patients with chronic thromboembolic pulmonary hypertension.Frontiers in immunology · 2024Article
- The role of foam cells in spinal cord injury: challenges and opportunities for intervention.Frontiers in immunology · 2024Review
- Different Pathways of Cellular Cholesterol Efflux.Cell biochemistry and biophysics · 2022Review
- Lack of ApoA-I in ApoEKO Mice Causes Skin Xanthomas, Worsening of Inflammation, and Increased Coronary Atherosclerosis in the Absence of Hyperlipidemia.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Cardiovascular disease in diabetes, beyond glucose.Cell metabolism · 2021Review
- Development of a non-invasive method for skin cholesterol detection: pre-clinical assessment in atherosclerosis screening.Biomedical engineering online · 2021Article
- Review
- Vascular Cells Proteome Associated with Bradykinin and Leptin Inflammation and Oxidative Stress Signals.Antioxidants (Basel, Switzerland) · 2020Article
- Site-specific 5-hydroxytryptophan incorporation into apolipoprotein A-I impairs cholesterol efflux activity and high-density lipoprotein biogenesis.The Journal of biological chemistry · 2020Article
- Article
- Anti-atherogenic effects of CD36-targeted epigallocatechin gallate-loaded nanoparticles.Journal of controlled release : official journal of the Controlled Release Society · 2019Article
- Administration of N-Acyl-Phosphatidylethanolamine Expressing Bacteria to Low Density Lipoprotein ReceptorScientific reports · 2019Article
- Protein markers of dysfunctional HDL in scavenger receptor class B type I deficient mice.Journal of translational medicine · 2018Article
- Apolipoprotein AI prevents regulatory to follicular helper T cell switching during atherosclerosis.Nature communications · 2018Article
- Apo A-I (Apolipoprotein A-I) Vascular Gene Therapy Provides Durable Protection Against Atherosclerosis in Hyperlipidemic Rabbits.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Threshold Effects of Circulating Angiopoietin-Like 3 Levels on Plasma Lipoproteins.The Journal of clinical endocrinology and metabolism · 2017Article
- Lipid-Free Apolipoprotein A-I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio.Journal of the American Heart Association · 2016Article
- Microdomains, Inflammation, and Atherosclerosis.Circulation research · 2016Review
- Procollagen C-endopeptidase Enhancer Protein 2 (PCPE2) Reduces Atherosclerosis in Mice by Enhancing Scavenger Receptor Class B1 (SR-BI)-mediated High-density Lipoprotein (HDL)-Cholesteryl Ester Uptake.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Tissue cholesterol accumulation, macrophage infiltration, and inflammation are features of atherosclerosis and some forms of dermatitis. HDL and its main protein, apoAI, are acceptors of excess cholesterol from macrophages; this process inhibits tissue inflammation. Recent epidemiologic and clinical trial evidence questions the role of HDL and its manipulation in cardiovascular disease. We investigated the effect of ectopic macrophage apoAI expression on atherosclerosis and dermatitis induced by the combination of hypercholesterolemia and absence of HDL in mice. Hematopoietic progenitor cells were transduced to express human apoAI and transplanted into lethally irradiated LDL receptor(-/-)/apoAI(-/-) mice, which were then placed on a high-fat diet for 16 weeks. Macrophage apoAI expression reduced aortic CD4(+) T-cell levels (-39.8%), lesion size (-25%), and necrotic core area (-31.6%), without affecting serum HDL or aortic macrophage levels. Macrophage apoAI reduced skin cholesterol by 39.8%, restored skin morphology, and reduced skin CD4(+) T-cell levels. Macrophage apoAI also reduced CD4(+) T-cell levels (-32.9%) in skin-draining lymph nodes but had no effect on other T cells, B cells, dendritic cells, or macrophages compared with control transplanted mice. Thus, macrophage apoAI expression protects against atherosclerosis and dermatitis by reducing cholesterol accumulation and regulating CD4(+) T-cell levels, without affecting serum HDL or tissue macrophage levels.
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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.