ArticleNature communications2016
The persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 2 of them syntheses that pooled it.
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
119 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Association of frailty and pre-frailty with cardiovascular mortality: a meta-analysis of 26 cohort studies.Frontiers in public health · 2025Pooled it
- Pooled it
- Oral and Intestinal Bacterial Substances Associated with Disease Activities in Patients with Rheumatoid Arthritis: A Cross-Sectional Clinical Study.Journal of immunology research · 2022Trial
- Trophoblast Extracellular Vesicles Rewire Immunity: A Symptom-Relief Avenue for Recessive Dystrophic Epidermolysis Bullosa.Journal of extracellular vesicles · 2026Article
- Smooth Muscle Cell Plasticity as a Central Determinant of Plaque Stability.Current atherosclerosis reports · 2026Review
- Chronic intermittent hypoxia sustains the low-grade inflammatory memory of monocytes via activation of myelopoiesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Differential regulation of monocyte exhaustion by distinct TLR agonists and underlying mechanisms.Cell communication and signaling : CCS · 2026Article
- Interleukin-1 Receptor-Associated Kinase 3 Attenuates Chondrocyte Senescence and Osteoarthritis via Inhibition of the TLR7/9-NF-κB Axis.Journal of molecular histology · 2026Article
- Modulatory Effects of Polyphenols on Altered Leukocyte Functions in Thromboinflammation and Diabetes Mellitus.International journal of molecular sciences · 2026Review
- Platelets as immune sensors: monitoring immune dynamics and diagnosing disease states across multiple disorders.EBioMedicine · 2026Article
- Trained immunity: new paradigm in the immunological memory of cardiovascular disease.ImmunoHorizons · 2026Review
- Sustained monocyte activation by persistent challenges with either oxLDL or free cholesterol and underlying mechanisms.ImmunoHorizons · 2026Article
- RUNX1-mediated repression of miR-24 promotes hepatic stellate cell activation and liver fibrosis by targeting the ALK4/Smad3 signaling pathway.Frontiers in genetics · 2026Article
- Inulin may inhibit ADAM17 to delay atherosclerosis.Open medicine (Warsaw, Poland) · 2026Article
- Propagation of monocyte exhaustion memory and underlying mechanisms.Cell communication and signaling : CCS · 2025Article
- Deciphering the immunomodulatory cross-talk: Bacterial extracellular vesicles in gut homeostasis.Virulence · 2025Review
- Cardiovascular inflammaging: Mechanisms, consequences, and therapeutic perspectives.Cell reports. Medicine · 2025Review
- Causal Relationship Between Serum Uric Acid and Atherosclerotic Disease: A Mendelian Randomization and Transcriptomic Analysis.Biomedicines · 2025Article
- Increased IFN responses drive myeloid cell activation in people living with HIV-1.Scientific reports · 2025Article
- Noncanonical feedback loop between "RIP3-MLKL" and "4EBP1-eIF4E" promotes neuronal necroptosis.MedComm · 2025Article
59 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Sustained low-grade inflammation mediated by non-resolving inflammatory monocytes has long been suspected in the pathogenesis of atherosclerosis; however, the molecular mechanisms responsible for the sustainment of non-resolving inflammatory monocytes during atherosclerosis are poorly understood. Here we observe that subclinical endotoxemia, often seen in humans with chronic inflammation, aggravates murine atherosclerosis through programming monocytes into a non-resolving inflammatory state with elevated Ly6C, CCR5, MCP-1 and reduced SR-B1. The sustainment of inflammatory monocytes is due to the disruption of homeostatic tolerance through the elevation of miR-24 and reduction of the key negative-feedback regulator IRAK-M. miR-24 reduces the levels of Smad4 required for the expression of IRAK-M and also downregulates key lipid-processing molecule SR-B1. IRAK-M deficiency in turn leads to elevated miR-24 levels, sustains disruption of monocyte homeostasis and aggravates atherosclerosis. Our data define an integrated feedback circuit in monocytes and its disruption may lead to non-resolving low-grade inflammation conducive to atherosclerosis.
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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.