Evidence map›Paper›PMID 24855059›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2014

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.

Ling Yan, Liby Mathew, Bijoy Chellan, Brandon Gardner, Judy Earley, Tipu S Puri, Marion A Hofmann Bowman

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023
    Review
  6. Article
  7. Article
  8. Article
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  11. Review
  12. Review
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  14. 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.] · 2018
    Article
  15. Article
  16. Review
  17. S100A8/A9 and sRAGE kinetic after polytrauma; an explorative observational study.Scandinavian journal of trauma, resuscitation and emergency medicine · 2017
    Observational
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Ling YanFrom the Department of Medicine, Cardiology (L.Y., B.C., B.G., J.E., M.A.H.B.) and Medicine, Nephrology (L.M., T.S.P.), The University of Chicago, IL.
Liby MathewFrom the Department of Medicine, Cardiology (L.Y., B.C., B.G., J.E., M.A.H.B.) and Medicine, Nephrology (L.M., T.S.P.), The University of Chicago, IL.
Bijoy ChellanFrom the Department of Medicine, Cardiology (L.Y., B.C., B.G., J.E., M.A.H.B.) and Medicine, Nephrology (L.M., T.S.P.), The University of Chicago, IL.
Brandon GardnerFrom the Department of Medicine, Cardiology (L.Y., B.C., B.G., J.E., M.A.H.B.) and Medicine, Nephrology (L.M., T.S.P.), The University of Chicago, IL.
Judy EarleyFrom the Department of Medicine, Cardiology (L.Y., B.C., B.G., J.E., M.A.H.B.) and Medicine, Nephrology (L.M., T.S.P.), The University of Chicago, IL.
Tipu S PuriFrom the Department of Medicine, Cardiology (L.Y., B.C., B.G., J.E., M.A.H.B.) and Medicine, Nephrology (L.M., T.S.P.), The University of Chicago, IL.
Marion A Hofmann BowmanFrom the Department of Medicine, Cardiology (L.Y., B.C., B.G., J.E., M.A.H.B.) and Medicine, Nephrology (L.M., T.S.P.), The University of Chicago, IL. mhofmann@medicine.bsd.uchicago.edu.
University of Chicago · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Pro-inflammatory S100 protein as disease modifier in calcific aortic valve diseasR01HL114821 · NHLBI · UNIVERSITY OF CHICAGO · PI HOFMANN BOWMAN, MARION A · 2012 to 2015
$1.5M
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR000430NHLBI NIH HHS 1R01HL4821NHLBI NIH HHS R01 HL114821
6 · The paper itself

Abstract

objectiveS100A12 and fibroblast growth factor 23 are biomarkers of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). We tested the hypothesis that human S100/calgranulin would accelerate cardiovascular disease in mice subjected to CKD. APPROACH AND

resultsA bacterial artificial chromosome of the human S100/calgranulin gene cluster containing the genes and regulatory elements for S100A8, S100A9, and S100A12 was expressed in C57BL/6J mouse (hBAC-S100) to generate a novel humanized mouse model. CKD was induced by ureteral ligation, and hBAC-S100 mice and wild-type mice were studied after 10 weeks of chronic uremia. hBAC-S100 mice with CKD showed increased fibroblast growth factor 23 in the hearts, left ventricular hypertrophy, diastolic dysfunction, focal cartilaginous metaplasia, and calcification of the mitral and aortic valve annulus together with aortic valve sclerosis. This phenotype was not observed in wild-type mice with CKD or in hBAC-S100 mice lacking the receptor for advanced glycation end products with CKD, suggesting that the inflammatory milieu mediated by S100/receptor for advanced glycation end products promotes pathological cardiac hypertrophy in CKD. In vitro, inflammatory stimuli including interleukin-6, tumor necrosis factor-α, lipopolysaccarides, or serum from hBAC-S100 mice upregulated fibroblast growth factor 23 mRNA and protein in primary murine neonatal and adult cardiac fibroblasts.

conclusionsMyeloid-derived human S100/calgranulin is associated with the development of cardiac hypertrophy and ectopic cardiac calcification in a receptor for advanced glycation end products-dependent manner in a mouse model of CKD. We speculate that fibroblast growth factor 23 produced by cardiac fibroblasts in response to cytokines may act in a paracrine manner to accelerate left ventricular hypertrophy and diastolic dysfunction in hBAC-S100 mice with CKD.

Indexed as

AnimalsAortic ValveCalcinosisCalgranulin ACalgranulin BCells, CulturedDiastoleDisease Models, AnimalFibroblast Growth Factor-23Fibroblast Growth FactorsFibroblastsGenotypeHeart Valve DiseasesHumansHypertrophy, Left VentricularInflammationCalgranulin ACalgranulin BFibroblast Growth Factor-23Fibroblast Growth FactorsInflammation MediatorsLeukocyte L1 Antigen ComplexReceptor for Advanced Glycation End ProductsReceptors, ImmunologicS100A12 ProteinS100A12 protein, humanS100 Proteinsglycosylation end products, advancedhypertrophy, left ventricularrenal insufficiency, chronicS100 proteins

Identifiers

PMID24855059
PMCPMC4108264
OpenAlexW2138130771

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.