Evidence map›Paper›PMID 39404904›Full record

ArticleBasic research in cardiology2024

Oxidative stress initiates hemodynamic change in CKD-induced heart disease.

Payel Sen, Jules Hamers, Theresa Sittig, Bachuki Shashikadze, Laura d'Ambrosio, Jan B Stöckl, Susanne Bierschenk, Hengliang Zhang, Chiara d'Alessio, Lotte M Zandbergen and 6 more

Abstract read
In one paragraph

Article in Basic research in cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. When in doubt, pig it out: a versatile translational platform to study CKD, HFpEF, and CKM syndrome.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
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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

16 authors.

Payel Sen *Institute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.ORCID 0000-0002-1613-7760
Jules Hamers *Institute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.ORCID 0000-0002-9715-2005
Theresa SittigInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.
Bachuki ShashikadzeGene Center, LMU Munich, Munich, Germany.ORCID 0000-0003-4558-0785
Laura d'AmbrosioInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.
Jan B StöcklGene Center, LMU Munich, Munich, Germany.
Susanne BierschenkInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.
Hengliang ZhangInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.ORCID 0000-0002-8174-7215
Chiara d'AlessioInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.
Lotte M ZandbergenInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.ORCID 0000-0001-6156-8095
Valerie PaulyInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.
Sebastian ClaussInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.ORCID 0000-0002-5675-6128
Eckhard WolfGene Center, LMU Munich, Munich, Germany.ORCID 0000-0002-0430-9510
Andreas DendorferInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany.ORCID 0000-0002-7806-312X
Thomas FröhlichGene Center, LMU Munich, Munich, Germany.ORCID 0000-0002-4709-3211
Daphne MerkusInstitute for Surgical Research, Walter Brendel Center of Experimental Medicine, University Clinic Munich, LMU Munich, Marchioninistrasse 68, 81377, Munich, Germany. daphne.merkus@med.uni-muenchen.de.ORCID 0000-0002-4852-831X

Funding

Chinese Government Scholarship CSC202108410141Dutch Cardiovascular Alliance 2020B008 RECONNEXTDZHK DZHK81Z0600207Friedrich Bauer Foundation 28/21
6 · The paper itself

Abstract

Chronic kidney disease (CKD) predisposes to cardiac remodeling and coronary microvascular dysfunction. Studies in swine identified changes in microvascular structure and function, as well as changes in mitochondrial structure and oxidative stress. However, CKD was combined with metabolic derangement, thereby obscuring the contribution of CKD alone. Therefore, we studied the impact of CKD on the heart and combined proteome studies with measurement of cardiac function and perfusion to identify processes involved in cardiac remodeling in CKD. CKD was induced in swine at 10-12 weeks of age while sham-operated swine served as controls. 5-6 months later, left ventricular (LV) function and coronary flow reserve were measured. LC-MS-MS-based proteomic analysis of LV tissue was performed. LV myocardium and kidneys were histologically examined for interstitial fibrosis and oxidative stress. Renal embolization resulted in mild chronic kidney injury (increased fibrosis and urinary NGAL). PV loops showed LV dilation and increased wall stress, while preload recruitable stroke work was impaired in CKD. Quantitative proteomic analysis of LV myocardium and STRING pre-ranked functional analysis showed enrichments in pathways related to contractile function, reactive oxygen species, and extracellular matrix (ECM) remodeling, which were confirmed histologically and associated with impaired total anti-oxidant capacity. H

Indexed as

Oxidative StressRenal Insufficiency, ChronicVentricular RemodelingAnimalsCoronary CirculationDisease Models, AnimalFibrosisHeart DiseasesHemodynamicsMyocardiumProteomicsSwineVentricular Function, LeftCardiac remodelingChronic kidney diseaseCoronary flow reserveOxidative stressProteomics

Identifiers

PMID39404904
PMCPMC11628585

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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.