ReviewToxins2019
New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease.
Review in Toxins, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Modulation of circulating osteocalcin-expressing monocytes by glucagon like peptide-1 receptor agonists in type 2 diabetes: an exploratory pilot study.Acta diabetologica · 2026Article
- Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Facile engineering of interactive double network hydrogels for heart valve regeneration.Nature communications · 2024Article
- Monocytes and Macrophages in Kidney Disease and Homeostasis.International journal of molecular sciences · 2024Review
- Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities.Biomolecules · 2024Review
- Serum HDL-C subfractions as predictors of cardiovascular calcification in hemodialysis patients: novel insights and clinical implications.Frontiers in medicine · 2024Article
- Chronic kidney disease is a key risk factor for aortic stenosis progression.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Article
- Leukocyte-endothelial interaction in CKD.Clinical kidney journal · 2023Review
- Inflammation-associated ectopic mineralization.Fundamental research · 2023Review
- Implications of uremic cardiomyopathy for the practicing clinician: an educational review.Heart failure reviews · 2023Review
- Contributions of bone marrow monocytes/macrophages in myeloproliferative neoplasms with JAK2Annals of hematology · 2023Article
- Article
- The Role of Iron in Calciphylaxis-A Current Review.Journal of clinical medicine · 2022Review
- Obesity, Diabetes Mellitus, and Vascular Impediment as Consequences of Excess Processed Food Consumption.Cureus · 2022Review
- Intracranial aneurysm calcification - A narrative review.Experimental neurology · 2022Review
- Association of Monocyte Count and Monocyte/Lymphocyte Ratio with the Risk of Cardiovascular Outcomes in Patients with CKD.Kidney360 · 2022Observational
- Tissue response, macrophage phenotype, and intrinsic calcification induced by cardiovascular biomaterials: Can clinical regenerative potential be predicted in a rat subcutaneous implant model?Journal of biomedical materials research. Part A · 2022Article
- Extracellular Vesicles From LPS-Treated Macrophages Aggravate Smooth Muscle Cell Calcification by Propagating Inflammation and Oxidative Stress.Frontiers in cell and developmental biology · 2022Article
- Contribution of Gut Microbiota-Derived Uremic Toxins to the Cardiovascular System Mineralization.Toxins · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC-particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.
Indexed as
Identifiers
What Socratic 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 Socratic graph.