Evidence map›Paper›PMID 38000021›Full record

ArticleScience advances2023

Mapping cardiac remodeling in chronic kidney disease.

Nadine Kaesler, Mingbo Cheng, James Nagai, James O'Sullivan, Fabian Peisker, Eric M J Bindels, Anne Babler, Julia Moellmann, Patrick Droste, Giulia Franciosa and 14 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. A platelet-monocyte pyroptotic axis mediates uremic cardiomyopathy: critical role of PF4 and hematopoietic caspase-1.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

24 authors at 8 institutions in 5 countries.

Nadine KaeslerClinic for Renal and Hypertensive Disorders, Rheumatological and Immunological Disease, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0001-8097-7660
Mingbo ChengInstitute for Computational Genomics, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0003-3938-0461
James NagaiInstitute for Computational Genomics, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0002-7655-7206
James O'SullivanCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.ORCID 0009-0002-3425-6058
Fabian PeiskerInstitute of Experimental Medicine and Systems Biology, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0003-0123-8179
Eric M J BindelsDepartment of Hematology, Erasmus Medical Center, Rotterdam, Netherlands.ORCID 0000-0001-9502-669X
Anne BablerInstitute of Experimental Medicine and Systems Biology, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0009-0006-7618-2025
Julia MoellmannDepartment of Internal Medicine I, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0002-8066-6114
Patrick DrosteClinic for Renal and Hypertensive Disorders, Rheumatological and Immunological Disease, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0001-9809-695X
Giulia FranciosaNovo Nordisk Foundation Center for Protein Research, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0001-5309-5558
Aurelien DugourdHeidelberg University, Faculty of Medicine, and Heidelberg University Hospital, Institute for Computational Biomedicine, Bioquant, Heidelberg, Germany.ORCID 0000-0002-0714-028X
Julio Saez-RodriguezHeidelberg University, Faculty of Medicine, and Heidelberg University Hospital, Institute for Computational Biomedicine, Bioquant, Heidelberg, Germany.ORCID 0000-0002-8552-8976
Sabine NeussInstitute of Pathology, University Hospital of the RWTH Aachen, Aachen, Germany.
Michael LehrkeDepartment of Internal Medicine I, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0003-2484-8068
Peter BoorClinic for Renal and Hypertensive Disorders, Rheumatological and Immunological Disease, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0001-9921-4284
Claudia GoettschDepartment of Internal Medicine I, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0002-7973-1329
Jesper V OlsenNovo Nordisk Foundation Center for Protein Research, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-4747-4938
Thimoteus SpeerDepartment of Medicine (Nephrology), Goethe University Frankfurt, Frankfurt, Germany.
Tzong-Shi LuBrigham and Women's Hospital, Renal Division, Boston, MA, USA.ORCID 0000-0002-3115-5000
Kenneth LimDivision of Nephrology and Hypertension, Indiana University School of Medicine, Indianapolis, IN, USA.
Jürgen FloegeClinic for Renal and Hypertensive Disorders, Rheumatological and Immunological Disease, University Hospital of the RWTH Aachen, Aachen, Germany.
Laura DenbyCentre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.ORCID 0000-0003-1277-708X
Ivan CostaInstitute for Computational Genomics, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0003-2890-8697
Rafael KramannClinic for Renal and Hypertensive Disorders, Rheumatological and Immunological Disease, University Hospital of the RWTH Aachen, Aachen, Germany.ORCID 0000-0003-4048-6351
RWTH Aachen University · DEErasmus MC · NLHeidelberg University · DEUniversity of Copenhagen · DKUniversity of Edinburgh · GBBrigham and Women's Hospital · USGoethe University Frankfurt · DEIndiana University School of Medicine

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with advanced chronic kidney disease (CKD) mostly die from sudden cardiac death and recurrent heart failure. The mechanisms of cardiac remodeling are largely unclear. To dissect molecular and cellular mechanisms of cardiac remodeling in CKD in an unbiased fashion, we performed left ventricular single-nuclear RNA sequencing in two mouse models of CKD. Our data showed a hypertrophic response trajectory of cardiomyocytes with stress signaling and metabolic changes driven by soluble uremia-related factors. We mapped fibroblast to myofibroblast differentiation in this process and identified notable changes in the cardiac vasculature, suggesting inflammation and dysfunction. An integrated analysis of cardiac cellular responses to uremic toxins pointed toward endothelin-1 and methylglyoxal being involved in capillary dysfunction and TNFα driving cardiomyocyte hypertrophy in CKD, which was validated in vitro and in vivo. TNFα inhibition in vivo ameliorated the cardiac phenotype in CKD. Thus, interventional approaches directed against uremic toxins, such as TNFα, hold promise to ameliorate cardiac remodeling in CKD.

Indexed as

Heart FailureRenal Insufficiency, ChronicAnimalsHumansMiceTumor Necrosis Factor-alphaUremic ToxinsVentricular RemodelingTumor Necrosis Factor-alphaUremic Toxins

Identifiers

PMID38000021
PMCPMC10672229
OpenAlexW4388966649

What Socratic holds

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LicenceCC BY-NC
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Registered trials

None linked

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.