ArticleScientific reports2017
The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 124 citations in OpenAlex.
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- Carotid plaque macrophage burden and inflammatory lipid-associated macrophage markers predict secondary major adverse cardiovascular events after endarterectomy.European heart journal · 2026Article
- Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis.Nature communications · 2026Article
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- Lipid nanoparticle-encapsulated DNA vaccine prevented lung consolidation following heterologous influenza A virus challenge in pigs.NPJ vaccines · 2026Article
- Tissue signatures of human macrophages during homeostasis and activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Estradiol treatment induces both shared and unique gene regulation and networks in adipose cell types of gonadectomized obese XX and XY mice.Biology of sex differences · 2026Article
- The effect of walnut consumption on the peripheral blood mononuclear cell transcriptome.Genes & nutrition · 2026Article
- Reframing macrophage polarization through cholesterol efflux: an organelle-coupled immunometabolic model.Frontiers in immunology · 2026Review
- Lnc-CHRM4-2:1 Inhibits M2 Polarization and Efferocytosis of Macrophages by Downregulating MerTK and SLC2A1 in Rheumatoid Arthritis.Journal of immunology research · 2026Article
- Identification of NR4A2 as a Potential Predictive Biomarker for Atherosclerosis.Combinatorial chemistry & high throughput screening · 2026Article
- Microbial allies in skin trauma recovery: from immune modulation to engineered probiotic therapeutics.Burns & trauma · 2026Review
- Efferocytosis-associated Mrc1Frontiers in immunology · 2026Article
- Inhibition of fatty acid-binding protein 4 alleviates psoriasis-like skin inflammation by modulating macrophage polarization.Frontiers in immunology · 2026Article
- Nutrient deprivation increases CD3 expression in RAW cells and augments the CD3-induced proinflammatory profile, associated with NFAT and IRF-1.Frontiers in immunology · 2026Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages play pivotal roles in the progression and regression of atherosclerosis. Accumulating evidence suggests that macrophage polarization into an anti-inflammatory M2 state is a key characteristic of atherosclerotic plaques undergoing regression. However, the molecular mechanisms underlying this potential association of the M2 polarization with atherosclerosis regression remain poorly understood. Further, human genetic factors that facilitate these anti-atherogenic processes remain largely unknown. We report that the transcription factor MafB plays pivotal roles in promoting macrophage M2 polarization. Further, MafB promotes cholesterol efflux from macrophage foam cells by directly up-regulating its key cellular mediators. Notably, MafB expression is significantly up-regulated in response to various metabolic and immunological stimuli that promote macrophage M2 polarization or cholesterol efflux, and thereby MafB mediates their beneficial effects, in both liver x receptor (LXR)-dependent and independent manners. In contrast, MafB is strongly down-regulated upon elevated pro-inflammatory signaling or by pro-inflammatory and pro-atherogenic microRNAs, miR-155 and miR-33. Using an integrative systems biology approach, we also revealed that M2 polarization and cholesterol efflux do not necessarily represent inter-dependent events, but MafB is broadly involved in both the processes. These findings highlight physiological protective roles that MafB may play against atherosclerosis progression.
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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 Socratic graph.