Evidence map›Paper›PMID 33753026›Full record

ArticleThe American journal of pathology2021

Promotion of β-Catenin/Forkhead Box Protein O Signaling Mediates Epithelial Repair in Kidney Injury.

Padmashree Rao, Xi Qiao, Winston Hua, Min Hu, Mariah Tahan, Titi Chen, Hong Yu, Xiaojun Ren, Qi Cao, Yiping Wang and 6 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The American journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The Role of Macrophages in Kidney Fibrosis.Frontiers in physiology · 2021
    Review
  9. Editorial: TGF-β in Human Disease: Friend or Foe?Frontiers in cell and developmental biology · 2021
    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

16 authors at 2 institutions in 2 countries.

Padmashree RaoCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Xi QiaoCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia; Department of Nephrology, Shanxi Medical University, Taiyuan, China.
Winston HuaCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Min HuCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Mariah TahanCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Titi ChenCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Hong YuCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Xiaojun RenCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia; Department of Nephrology, Shanxi Medical University, Taiyuan, China.
Qi CaoCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Yiping WangCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Ying YangCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia; Department of Nephrology, Shanxi Medical University, Taiyuan, China.
Yuan M WangCentre for Kidney Research Children's Hospital at Westmead, Australia.
Vincent W LeeCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia; Department of Nephrology, Westmead Hospital, Australia.
Stephen I AlexanderCentre for Kidney Research Children's Hospital at Westmead, Australia.
David C HarrisCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia; Department of Nephrology, Westmead Hospital, Australia.
Guoping ZhengCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia. Electronic address: guoping.zheng@sydney.edu.au.
The University of Sydney · AUChildren's Hospital at Westmead · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is characterized by progressively excessive deposition of matrix components and may lead to organ failure. Transforming growth factor-β (TGF-β) is a key cytokine involved in tissue repair and fibrosis. TGF-β's profibrotic signaling pathways converge at activation of β-catenin. β-Catenin is an important transcription cofactor whose function depends on its binding partner. Promoting β-catenin binding to forkhead box protein O (Foxo) via inhibition of its binding to T-cell factor (TCF) reduces kidney fibrosis in experimental murine models. Herein, we investigated whether β-catenin/Foxo diverts TGF-β signaling from profibrotic to physiological epithelial healing. In an in vitro model of wound healing (scratch assay), and in an in vivo model of kidney injury, unilateral renal ischemia reperfusion, TGF-β treatment in combination with either ICG-001 or iCRT3 (β-catenin/TCF inhibitors) increased β-catenin/Foxo interaction, increased scratch closure by increased cell proliferation and migration, reduced the TGF-β-induced mesenchymal differentiation, and healed the ischemia reperfusion injury with less fibrosis. In addition, administration of ICG-001 or iCRT3 reduced the contractile activity induced by TGF-β in C1.1 cells. Together, our results indicate that redirection of β-catenin binding from TCF to Foxo promotes β-catenin/Foxo-mediated epithelial repair. Targeting β-catenin/Foxo may rebuild normal structure of injured kidney.

Indexed as

Animalsbeta CateninFibrosisForkhead Box Protein O1Kidney DiseasesMiceSignal TransductionWound Healingbeta CateninForkhead Box Protein O1

Identifiers

PMID33753026
PMCPMC8351131
OpenAlexW3137108037

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.