Evidence map›Paper›PMID 32369448›Full record

ArticleJCI insight2020

Tubular β-catenin and FoxO3 interactions protect in chronic kidney disease.

Stellor Nlandu-Khodo, Yosuke Osaki, Lauren Scarfe, Haichun Yang, Melanie Phillips-Mignemi, Jane Tonello, Kenyi Saito-Diaz, Surekha Neelisetty, Alla Ivanova, Tessa Huffstater and 7 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  10. Assays to enhance metabolic phenotyping in the kidney.American journal of physiology. Renal physiology · 2025
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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

17 authors at 7 institutions in 3 countries.

Stellor Nlandu-KhodoDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Yosuke OsakiDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Lauren ScarfeDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Haichun YangDepartment of Pathology, Microbiology and Immunology, VUMC, Nashville, Tennessee, USA.
Melanie Phillips-MignemiDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Jane TonelloDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Kenyi Saito-DiazDepartment of Cell and Developmental Biology and.
Surekha NeelisettyDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Alla IvanovaDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Tessa HuffstaterDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee, USA.
Robert McMahonDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
M Mark TaketoDivision of Experimental Therapeutics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Mark deCaesteckerDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Balakuntalam KasinathDepartment of Medicine, Long School of Medicine, University of Texas Health San Antonio, San Antonio, Texas, USA.
Raymond C HarrisDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Ethan LeeDepartment of Cell and Developmental Biology and.
Leslie S GewinDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center (VUMC), Nashville, Tennessee, USA.
Vanderbilt University Medical Center · USVanderbilt University · USKyoto University · JPTennessee Clinical Research Center · USThe University of Texas Health Science Center at San Antonio · USUniversity of Zurich · CHVA Tennessee Valley Healthcare System · US

Funding

The Role of the EGF Receptor in Acute and Chronic Renal InjuryR01DK051265 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 1997 to 2026
$10.1M
Vanderbilt O'Brien Kidney Center - Core D - Clinical and Translational CoreP30DK114809 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRIS, RAYMOND C., POZZI, AMBRA · 2017 to 2021
$5.9M
Mechanism of Wnt signal transductionR35GM122516 · NIGMS · VANDERBILT UNIVERSITY · PI ETHAN LEE · 2017 to 2026
$5.8M
TGF-beta Pathways that Protect Epithelia in Chronic Renal InjuryR01DK108968 · NIDDK · WASHINGTON UNIVERSITY · PI GEWIN, LESLIE S · 2016 to 2025
$3.7M
Mechanisms and therapeutic manipulation of retinoic acid signaling in Acute Kidney InjuryR01DK112688 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DE CAESTECKER, MARK P. · 2017 to 2020
$1.7M
The Role of Fatty Acid Oxidation in Injured Kidney TubulesI01BX003425 · VA · VETERANS HEALTH ADMINISTRATION · PI Leslie S Gewin · 2018 to 2026
–
BLRD VA I01 BX001340BLRD VA I01 BX003425NIDDK NIH HHS P30 DK114809NIDDK NIH HHS R01 DK051265NIDDK NIH HHS R01 DK108968NIDDK NIH HHS R01 DK112688NIGMS NIH HHS R35 GM122516
6 · The paper itself

Abstract

The Wnt/β-catenin signaling pathway plays an important role in renal development and is reexpressed in the injured kidney and other organs. β-Catenin signaling is protective in acute kidney injury (AKI) through actions on the proximal tubule, but the current dogma is that Wnt/β-catenin signaling promotes fibrosis and development of chronic kidney disease (CKD). As the role of proximal tubular β-catenin signaling in CKD remains unclear, we genetically stabilized (i.e., activated) β-catenin specifically in murine proximal tubules. Mice with increased tubular β-catenin signaling were protected in 2 murine models of AKI to CKD progression. Oxidative stress, a common feature of CKD, reduced the conventional T cell factor/lymphoid enhancer factor-dependent β-catenin signaling and augmented FoxO3-dependent activity in proximal tubule cells in vitro and in vivo. The protective effect of proximal tubular β-catenin in renal injury required the presence of FoxO3 in vivo. Furthermore, we identified cystathionine γ-lyase as a potentially novel transcriptional target of β-catenin/FoxO3 interactions in the proximal tubule. Thus, our studies overturned the conventional dogma about β-catenin signaling and CKD by showing a protective effect of proximal tubule β-catenin in CKD and identified a potentially new transcriptional target of β-catenin/FoxO3 signaling that has therapeutic potential for CKD.

Indexed as

Signal TransductionAcute Kidney InjuryAnimalsbeta CateninForkhead Box Protein O3Kidney Tubules, ProximalMaleMiceMice, TransgenicRenal Insufficiency, Chronicbeta CateninForkhead Box Protein O3FoxO3 protein, mouseCell BiologyCell stressFibrosisNephrology

Identifiers

PMID32369448
PMCPMC7259539
OpenAlexW3023647415

What OpenQuestion holds

Textmetadata
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.