ArticlePloS one2014
Uremic conditions drive human monocytes to pro-atherogenic differentiation via an angiotensin-dependent mechanism.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03231410 (Role of Monocytes Adhesion and Vascular Lesions in Vascular Access Success or Failure in Uremic Patients), which is not on this map. Cited by 20 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.
Role of Monocytes Adhesion and Vascular Lesions in Vascular Access Success or Failure in Uremic Patients
Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Impaired function and delayed regeneration of dendritic cells in COVID-19.PLoS pathogens · 2021Trial
- ACE/ACE2 axis in cardiovascular disease and COVID-19: Molecular insights and therapeutic perspectives.Journal of cardiovascular and thoracic research · 2026Review
- Inflammatory markers mediate association of AIP with kidney failure risk: data from National Health and Nutrition Examination Survey (NHANES) 2005-2018.Renal failure · 2025Article
- Cellular and molecular mechanisms underlying hemodialysis arteriovenous fistula dysfunction and approaches to promote maturation: a vascular perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Aprotinin (I): Understanding the Role of Host Proteases in COVID-19 and the Importance of Pharmacologically Regulating Their Function.International journal of molecular sciences · 2024Review
- APP-CD74 axis mediates endothelial cell-macrophage communication to promote kidney injury and fibrosis.Frontiers in pharmacology · 2024Article
- Research Progress of Flavonoids Regulating Endothelial Function.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Uremic Toxins Induce THP-1 Monocyte Endothelial Adhesion and Migration through Specific miRNA Expression.International journal of molecular sciences · 2023Article
- Angiotensin Converting Enzyme 1 Expression in the Leukocytes of Adults Aged 64 to 67 Years.JMIRx med · 2023Article
- Histology and Immunohistochemistry of Radial Arteries Are Suggestive of an Interaction between Calcification and Early Atherosclerotic Lesions in Chronic Kidney Disease.Medicina (Kaunas, Lithuania) · 2021Article
- Macrophage and adipocyte interaction as a source of inflammation in kidney disease.Scientific reports · 2021Observational
- Article
- Review
- Monocytes in Uremia.Toxins · 2020Review
- 25-vitamin D reduces inflammation in uremic environment.Scientific reports · 2020Article
- Role of angiotensin-converting enzyme in myeloid cell immune responses.Cellular & molecular biology letters · 2020Review
- Altered monocytic phenotypes are linked with systemic inflammation and may be linked to mortality in dialysis patients.Scientific reports · 2019Article
- Indoxyl sulfate (IS)-mediated immune dysfunction provokes endothelial damage in patients with end-stage renal disease (ESRD).Scientific reports · 2017Article
- Monocytic angiotensin-converting enzyme 2 relates to atherosclerosis in patients with chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsElevated expression levels of monocytic-ACE have been found in haemodialysis patients. They are not only epidemiologically linked with increased mortality and cardiovascular disease, but may also directly participate in the initial steps of atherosclerosis. To further address this question we tested the role of monocytic-ACE in promotion of atherosclerotic events in vitro under conditions mimicking those of chronic renal failure. METHODS AND
resultsTreatment of human primary monocytes or THP-1 cells with uremic serum as well as PMA-induced differentiation led to significantly up-regulated expression of ACE, further increased by additional treatment with LPS. Functionally, these monocytes revealed significantly increased adhesion and transmigration through endothelial monolayers. Overexpression of ACE in transfected monocytes or THP-1 cells led to development of more differentiated, macrophage-like phenotype with up-regulated expression of Arg1, MCSF, MCP-1 and CCR2. Expression of pro-inflammatory cytokines TNFa and IL-6 were also noticeably up-regulated. ACE overexpression resulted in significantly increased adhesion and transmigration properties. Transcriptional screening of ACE-overexpressing monocytes revealed noticeably increased expression of Angiotensin II receptors and adhesion- as well as atherosclerosis-related ICAM-1 and VCAM1. Inhibition of monocyte ACE or AngII-receptor signalling led to decreased adhesion potential of ACE-overexpressing cells.
conclusionsTaken together, these data demonstrate that uremia induced expression of monocytic-ACE mediates the development of highly pro-atherogenic cells via an AngII-dependent mechanism.
Indexed as
Identifiers
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.