ArticleCirculation2011
S100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells: implications for atherosclerosis and adipose tissue inflammation.
Article in Circulation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis 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
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.
- Circulating Levels of Calprotectin as a Biomarker in Patients With Coronary Artery Disease: A Systematic Review and Meta-Analysis.Clinical cardiology · 2024Pooled it
- Trial
- Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment.Signal transduction and targeted therapy · 2026Article
- Exploring the Relevance of S100A8 and S100A9 Proteins in Preeclampsia: A Narrative Review.International journal of molecular sciences · 2025Review
- Characterizing the effect of bariatric surgery on circulating S100A9.International journal of obesity (2005) · 2025Article
- Single-cell atlas of human liver and blood immune cells across fatty liver disease stages reveals distinct signatures linked to liver dysfunction and fibrogenesis.Nature immunology · 2025Article
- Adiposome Proteomics Uncover Molecular Signatures of Cardiometabolic Risk in Obese Individuals.Proteomes · 2025Article
- The metabolic advantage of being young and male in obesity treatment outcomes in mice.npj metabolic health and disease · 2025Article
- Shared Mechanisms in Cancer and Cardiovascular Disease: S100A8/9 and the NLRP3 Inflammasome: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- Immune-related diagnostic indicators and targeted therapies for COPD combined with NASH were identified and verified via WGCNA and LASSO.Frontiers in immunology · 2025Article
- The role of calprotectin in giant cell arteritis - from pathophysiology to possible clinical applications.Frontiers in immunology · 2025Review
- RE: Proteomic Exploration of Potential Blood Biomarkers in Haemophilic Arthropathy.Health science reports · 2024Article
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- Identification of Transcriptomic Signatures of Pancreatic Ductal Adenocarcinoma-Derived Exosomes That Promote Macrophage M2 Polarization and Predict Prognosis: S100A9 Reveals Tumor Progression.Clinical Medicine Insights. Oncology · 2024Article
- Western-style diet in the presence of elevated circulating testosterone induces adipocyte hypertrophy without proinflammatory responses in rhesus macaques.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- S100a9 Protects Against the Effects of Repeated Social Defeat Stress.Biological psychiatry global open science · 2023Article
- Pleiotrophin drives a prometastatic immune niche in breast cancer.The Journal of experimental medicine · 2023Article
- An immunometabolism subtyping system identifies S100A9Cell reports. Medicine · 2023Article
- Kidney stone matrix proteins: Role in stone formation.World journal of nephrology · 2023Review
- Quantitative proteomic landscape of unstable atherosclerosis identifies molecular signatures and therapeutic targets for plaque stabilization.Communications biology · 2023Article
32 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
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundS100A9 is constitutively expressed in neutrophils, dendritic cells, and monocytes; is associated with acute and chronic inflammatory conditions; and is implicated in obesity and cardiovascular disease in humans. Most of the constitutively secreted S100A9 is derived from myeloid cells. A recent report demonstrated that mice deficient in S100A9 exhibit reduced atherosclerosis compared with controls and suggested that this effect was due in large part to loss of S100A9 in bone marrow-derived cells. METHODS AND
resultsTo directly investigate the role of bone marrow-derived S100A9 in atherosclerosis and insulin resistance in mice, low-density lipoprotein receptor-deficient, S100A9-deficient bone marrow chimeras were generated. Neither atherosclerosis nor insulin resistance was reduced in S100A9-deficient chimeras fed a diet rich in fat and carbohydrates. To investigate the reason for this lack of effect, myeloid cells were isolated from the peritoneal cavity or bone marrow. S100A9-deficient neutrophils exhibited a reduced secretion of cytokines in response to toll-like receptor-4 stimulation. In striking contrast, S100A9-deficient dendritic cells showed an exacerbated release of cytokines after toll-like receptor stimulation. Macrophages rapidly lost S100A9 expression during maturation; hence, S100A9 deficiency did not affect the inflammatory status of macrophages.
conclusionsS100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells. The effect of S100A9 deficiency on atherosclerosis and other inflammatory diseases is therefore predicted to depend on the relative contribution of these cell types at different stages of disease progression. Furthermore, S100A9 expression in nonmyeloid cells is likely to contribute to atherosclerosis.
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What OpenQuestion holds
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.