Evidence map›Paper›PMID 24652804›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

TGF-β-activated kinase 1 is crucial in podocyte differentiation and glomerular capillary formation.

Sung Il Kim, So-Young Lee, Zhibo Wang, Yan Ding, Nadeem Haque, Jiwang Zhang, Jing Zhou, Mary E Choi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Inhibition of eCIRP attenuates PANoptosis and renal fibrosis.American journal of physiology. Renal physiology · 2025
    Article
  2. The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025
    Review
  3. Review
  4. Article
  5. Gene regulatory networks in disease and ageing.Nature reviews. Nephrology · 2024
    Review
  6. Article
  7. TAK1 in Vascular Signaling: "Friend or Foe"?Journal of inflammation research · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Glomerular cell crosstalk.Current opinion in nephrology and hypertension · 2016
    Review
  12. TGF-β signaling in the kidney: profibrotic and protective effects.American journal of physiology. Renal physiology · 2016
    Review
  13. Article
  14. Crosstalk in glomerular injury and repair.Current opinion in nephrology and hypertension · 2015
    Review
  15. Article
  16. Therapeutic targets for treating fibrotic kidney diseases.Translational research : the journal of laboratory and clinical medicine · 2015
    Review
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

8 authors at 4 institutions in 1 country.

Sung Il KimRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Division of Nephrology and Hypertension, Weill Cornell Medical College, New York, New York; szk2006@med.cornell.edu mechoi@med.cornell.edu.
So-Young LeeRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Internal Medicine, Bundang CHA Medical Center, CHA University School of Medicine, Seongnam, South Korea; and.
Zhibo WangRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Yan DingRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Division of Nephrology and Hypertension, Weill Cornell Medical College, New York, New York;
Nadeem HaqueRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Jiwang ZhangOncology Institute, Cardinal Bernardin Cancer Center, Department of Pathology, Loyola University Medical Center, Maywood, Illinois.
Jing ZhouRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Mary E ChoiRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Division of Nephrology and Hypertension, Weill Cornell Medical College, New York, New York; szk2006@med.cornell.edu mechoi@med.cornell.edu.
Brigham and Women's Hospital · USHarvard University · USCornell University · USLoyola University Medical Center · US

Funding

TGF-beta signaling in the kidneyR01DK057661 · NIDDK · YALE UNIVERSITY · PI CHOI, MARY E · 2000 to 2014
$4.1M
NIDDK NIH HHS R01 DK057661NIDDK NIH HHS R01-DK57661
6 · The paper itself

Abstract

TGF-β-activated kinase 1 (TAK1) is a key intermediate in signal transduction induced by TGF-β or inflammatory cytokines, such as TNF-α and IL-1, which are potent inducers of podocyte injury responses that lead to proteinuria and glomerulosclerosis. Nevertheless, little is known about the physiologic and pathologic roles of TAK1 in podocytes. To examine the in vivo role of TAK1, we generated podocyte-specific Tak1 knockout mice (Nphs2-Cre(+):Tak1(fx/fx); Tak1(∆/∆)). Targeted deletion of Tak1 in podocytes resulted in perinatal lethality, with approximately 50% of animals dying soon after birth and 90% of animals dying within 1 week of birth. Tak1(∆/∆) mice developed proteinuria from P1 and exhibited delayed glomerulogenesis and reduced expression of Wilms' tumor suppressor 1 and nephrin in podocytes. Compared with Tak1(fx/fx) mice, Tak1(∆/∆) mice exhibited impaired formation of podocyte foot processes that caused disruption of the podocyte architecture with prominent foot process effacement. Intriguingly, Tak1(∆/∆) mice displayed increased expression of vascular endothelial growth factor within the glomerulus and abnormally enlarged glomerular capillaries. Furthermore, 4- and 7-week-old Tak1(∆/∆) mice with proteinuria had increased collagen deposition in the mesangium and the adjacent tubulointerstitial area. Thus, loss of Tak1 in podocytes is associated with the development of proteinuria and glomerulosclerosis. Taken together, our data show that TAK1 regulates the expression of Wilms' tumor suppressor 1, nephrin, and vascular endothelial growth factor and that TAK1 signaling has a crucial role in podocyte differentiation and attainment of normal glomerular microvasculature during kidney development and glomerular filtration barrier homeostasis.

Indexed as

AnimalsAnimals, NewbornCapillariesCell DifferentiationCollagenFemaleGlomerular Filtration BarrierKidney GlomerulusMaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutPodocytesCollagenMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMembrane ProteinsnephrinRNA, MessengerVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseWT1 Proteins

Identifiers

PMID24652804
PMCPMC4147968
OpenAlexW2111777313

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.