ArticleAmerican journal of nephrology2011
Vascular remodeling and arterial calcification are directly mediated by S100A12 (EN-RAGE) in chronic kidney disease.
Article in American journal of nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 64 citations in OpenAlex.
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- Article
- The Gly82Ser polymorphism in the receptor for advanced glycation endproducts increases the risk for coronary events in the general population.Scientific reports · 2024Article
- Immunological mechanisms underlying sterile inflammation in the pathogenesis of atherosclerosis: potential sites for intervention.Expert review of clinical immunology · 2021Review
- Regulation of Vascular Calcification by Reactive Oxygen Species.Antioxidants (Basel, Switzerland) · 2020Review
- Role of Advanced Glycation End Products on Aortic Calcification in Patients with Type 2 Diabetes Mellitus.Journal of clinical medicine · 2020Article
- World Trade Center-Cardiorespiratory and Vascular Dysfunction: Assessing the Phenotype and Metabolome of a Murine Particulate Matter Exposure Model.Scientific reports · 2020Article
- Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models.Frontiers in cardiovascular medicine · 2020Review
- sRAGE attenuates angiotensin II-induced cardiomyocyte hypertrophy by inhibiting RAGE-NFκB-NLRP3 activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Review
- S100/RAGE-Mediated Inflammation and Modified Cholesterol Lipoproteins as Mediators of Osteoblastic Differentiation of Vascular Smooth Muscle Cells.Frontiers in cardiovascular medicine · 2018Review
- Vascular Calcification: Current Genetics Underlying This Complex Phenomenon.Chinese medical journal · 2017Review
- Arterial Calcification in Diabetes Mellitus: Preclinical Models and Translational Implications.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins.Cellular & molecular immunology · 2017Review
- The Biology of Hemodialysis Vascular Access Failure.Seminars in interventional radiology · 2016Review
- Circulating S100A12 Levels Are Associated with Progression of Abdominal Aortic Calcification in Hemodialysis Patients.PloS one · 2016Article
- S100A12 and the S100/Calgranulins: Emerging Biomarkers for Atherosclerosis and Possibly Therapeutic Targets.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Serum soluble RAGE levels and carotid atherosclerosis: the Northern Manhattan Study (NOMAS).Atherosclerosis · 2015Article
- Article
- S100/Calgranulin-mediated inflammation accelerates left ventricular hypertrophy and aortic valve sclerosis in chronic kidney disease in a receptor for advanced glycation end products-dependent manner.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
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
Abstract
backgroundThe proinflammatory cytokine S100A12 (also known as EN-RAGE) is associated with cardiovascular morbidity and mortality in hemodialysis patients. In the current study, we tested the hypothesis that S100A12 expressed in vascular smooth muscle in nonatherosclerosis-prone C57BL/6J mice on normal rodent chow diet, but exposed to the metabolic changes of chronic kidney disease (CKD), would develop vascular disease resembling that observed in patients with CKD.
methodsCKD was induced in S100A12 transgenic mice and wild-type littermate mice not expressing human S100A12 by surgical ligation of the ureters. The aorta was analyzed after 7 weeks of elevated BUN (blood urea nitrogen), and cultured aortic smooth muscle cells were studied.
resultsWe found enhanced vascular medial calcification in S100A12tg mice subjected to CKD. Vascular calcification was mediated, at least in part, by activation of the receptor for S100A12, RAGE (receptor for advanced glycation endproducts), and by enhanced oxidative stress, since inhibition of NADPH-oxidase Nox1 and limited access of S100A12 to RAGE attenuated the calcification and gene expression of osteoblastic genes in cultured vascular smooth muscle cells.
conclusionS100A12 augments CKD-triggered osteogenesis in murine vasculature, reminiscent of features associated with enhanced vascular calcification in patients with chronic and end-stage kidney disease.
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.