Evidence map›Paper›PMID 26312158›Full record

ReviewKidney international supplements2014

Role of HIPK2 in kidney fibrosis.

Ying Fan, Niansong Wang, Peter Chuang, John C He

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney international supplements, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Research progress in anti-renal fibrosis drugs.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Loss of HIPK2 Protects Neurons from Mitochondrial Toxins by Regulating Parkin Protein Turnover.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. HIPK2-Mediated Transcriptional Control of NMDA Receptor Subunit Expression Regulates Neuronal Survival and Cell Death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    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

4 authors at 2 institutions in 2 countries.

Ying FanDepartment of Nephrology, Shanghai 6th People's Hospital affiliated to Shanghai Jiaotong University , Shanghai, China.
Niansong WangDepartment of Nephrology, Shanghai 6th People's Hospital affiliated to Shanghai Jiaotong University , Shanghai, China.
Peter ChuangDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai , New York, New York, USA.
John C HeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai , New York, New York, USA.
Icahn School of Medicine at Mount Sinai · USShanghai Jiao Tong University · CN

Funding

Role of HIPK2 in Kidney Tubulointerstitial InjuryR01DK088541 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2010 to 2019
$4.0M
NIDDK NIH HHS R01 DK088541
6 · The paper itself

Abstract

Homeodomain interacting protein kinase 2 (HIPK2) functions as either a co-repressor or a co-activator of transcriptional regulators. Dysregulation of HIPK2 is associated with cancer and neurological disease. Recently, we found that HIPK2 is also an important driver of kidney fibrosis in the HIV-1 transgenic murine model, Tg26. HIPK2 protein levels are upregulated in the tubular epithelial cells of Tg26 mice as well as in kidney biopsies of patients with HIV-associated nephropathy, focal segmental glomerulosclerosis, diabetic nephropathy, and IgA nephropathy. We found that HIPK2 regulates pro-apoptotic, pro-fibrotic, and pro-inflammatory pathways including p53, transforming growth factor β (TGF-β)-SMAD family member 3 (Smad3), Notch, Wingless and INT-1 (Wnt)/β-catenin, and nuclear factor kappa-light-chain-enhancer of activated B cells in renal tubular epithelial cells. Our data suggest that HIPK2 may be a potential target for antifibrotic therapy. As mice with germline deletion of

Indexed as

cell signalingHIPK2kidney fibrosistubular epithelial cell

Identifiers

PMID26312158
PMCPMC4536960
OpenAlexW2080672043

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.