Evidence map›Paper›PMID 30158457›Full record

ArticleInternational journal of molecular sciences2018

Telocinobufagin, a Novel Cardiotonic Steroid, Promotes Renal Fibrosis via Na⁺/K⁺-ATPase Profibrotic Signaling Pathways.

David J Kennedy, Fatimah K Khalaf, Brendan Sheehy, Malory E Weber, Brendan Agatisa-Boyle, Julijana Conic, Kayla Hauser, Charles M Medert, Kristen Westfall, Philip Bucur and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Exploring the Mechanism of NabioRxiv : the preprint server for biology · 2026
    Article
  2. Molecular mechanisms of ovarian fibrosis.Molecular human reproduction · 2026
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  11. Microcystin-LR (MC-LR) Triggers Inflammatory Responses in Macrophages.International journal of molecular sciences · 2021
    Article
  12. Article
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  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

13 authors at 5 institutions in 2 countries.

David J KennedyDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH 43614, USA. David.Kennedy@UToledo.edu.ORCID 0000-0001-5265-0142
Fatimah K KhalafDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH 43614, USA. kareem.khalaf@rockets.utoledo.edu.
Brendan SheehyDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. bts21@case.edu.
Malory E WeberDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. weberm9@ccf.org.
Brendan Agatisa-BoyleDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. bcaboyle@gmail.com.
Julijana ConicDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. julijanaconic@gmail.com.
Kayla HauserDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. kvmislick@gmail.com.
Charles M MedertDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. c.maxmedert@gmail.com.
Kristen WestfallDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. WESTFAK@ccf.org.
Philip BucurDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. pb403014@ohio.edu.
Olga V FedorovaLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. FedorovO@grc.nia.nih.gov.
Alexei Y BagrovSechenov Institute of Evolutionary Physiology and Biochemistry, St. Petersburg 194223, Russia. aybagrov@gmail.com.
W H Wilson TangDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, OH 44106, USA. tangw@ccf.org.
Cleveland Clinic Lerner College of Medicine · USUniversity of Toledo · USCleveland Clinic · USInstitute of Evolutionary Physiology and Biochemistry · RUNational Institutes of Health · US

Funding

Sodium pump ligands in blood pressure regulation and profibrotic signaling in hypertension, chronic kidney disease and aging in males and femalesZIAAG000609 · NIA · NATIONAL INSTITUTE ON AGING · PI FEDOROVA, OLGA V · 2009 to 2025
$17.3M
Marinobufagenin as a therapeutic targetZIAAG000869 · NIA · NATIONAL INSTITUTE ON AGING · PI LAKATTA, EDWARD · 2009 to 2025
$14.8M
Diet, Gut Microbiota, and Heart FailureR01HL126827 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L, TANG, WAI HONG WILSON · 2016 to 2019
$3.1M
Counter regulatory mechanisms of cardiotonic steroids in cardio-renal syndromeR01HL137004 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI KENNEDY, DAVID JOSEPH · 2017 to 2021
$1.9M
American Heart Association 14SDG18650010National Institutes of Health P20HL113452National Institutes of Health R01DK106000National Institutes of Health R01HL103931National Institutes of Health R01HL105649National Institutes of Health R01HL126827National Institutes of Health R01HL137004National Institutes of Health UL1TR000439NHLBI NIH HHS R01 HL126827NHLBI NIH HHS R01 HL137004Russian Science Foundation 18-15-00222
6 · The paper itself

Abstract

Cardiotonic steroids (CTS) are Na⁺/K⁺-ATPase (NKA) ligands that are elevated in volume-expanded states and associated with cardiac and renal dysfunction in both clinical and experimental settings. We test the hypothesis that the CTS telocinobufagin (TCB) promotes renal dysfunction in a process involving signaling through the NKA α-1 in the following studies. First, we infuse TCB (4 weeks at 0.1 µg/g/day) or a vehicle into mice expressing wild-type (WT) NKA α-1, as well as mice with a genetic reduction (~40%) of NKA α-1 (NKA α-1

Indexed as

AnimalsBufanolidesCell LineFibrosisGlycogen Synthase Kinase 3 betaKidney DiseasesMAP Kinase Signaling SystemMiceOuabainPhosphorylationSignal TransductionSodium-Potassium-Exchanging ATPaseSwineBufanolidesGlycogen Synthase Kinase 3 betamarinobufageninOuabainSodium-Potassium-Exchanging ATPasetelocinobufagincardiotonic steroidsfibrosiskidneyNa+/K+-ATPasesignalingtelocinobufagin

Identifiers

PMID30158457
PMCPMC6164831
OpenAlexW2889489827

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.