Evidence map›Paper›PMID 26035380›Full record

ArticleDisease models & mechanisms2015

IKKα is involved in kidney recovery and regeneration of acute ischemia/reperfusion injury in mice through IL10-producing regulatory T cells.

Xin Wan, Li-Jun Hou, Li-Yuan Zhang, Wen-Juan Huang, Lin Liu, Qian Zhang, Bo Hu, Wen Chen, Xin Chen, Chang-Chun Cao

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2015. 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
1.1field-weighted citation impact, top 20% 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, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Inhibitory Effects of Rhein on Renal Interstitial Fibrosis via the SHH-Gli1 Signal Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  5. Review
  6. Article
  7. Deficiency of IKKJournal of immunology research · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. HyperpolarizedNMR in biomedicine · 2017
    Article
  16. 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

10 authors at 2 institutions in 1 country.

Xin WanDivision of Nephrology, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Li-Jun HouDivision of Neurosurgery, Department of Surgery and Shanghai Neurosurgical Institute, The Second Military Medical University, Changzheng Hospital, Shanghai 200003, China.
Li-Yuan ZhangDivision of Nephrology, Department of Medicine, Affiliated Lianyungang Clinical Medical College of Nanjing Medical University, Lianyungang 222002, China.
Wen-Juan HuangDivision of Nephrology, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Lin LiuDivision of Nephrology, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Qian ZhangDivision of Nephrology, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Bo HuDivision of Nephrology, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Wen ChenDivision of Cardiovascular Surgery, Department of Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Xin ChenDivision of Cardiovascular Surgery, Department of Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Chang-Chun CaoDivision of Nephrology, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China caochangchun@njmu.edu.cn.
Nanjing Medical University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recovery phase after kidney ischemia/reperfusion (IR) injury is often associated with the suppression of inflammation and the proliferation of tubular epithelial cells (TECs). The duration of this phase is often determined by the suppression of inflammation and the proliferation of TECs. Several lines of evidence suggest that IκB kinase α (IKKα) not only promotes the production of anti-inflammatory factors and/or prevents the production of inflammatory factors, but also induces the accompanying cell differentiation and regeneration, and suppresses inflammation. We therefore hypothesized that IKKα could participate in the kidney repair after IR injury and have used a mouse model of acute kidney injury (AKI) to test this. We found that IKKα mediated the repair of the kidney via infiltrated regulatory T (Treg) cells, which can produce anti-inflammatory cytokine IL10, and that IKKα also increased the proliferation of the surviving TECs and suppressed of inflammation. In addition, the expression of indoleamine 2,3-dioxygenase (IDO) in TECs is consistent with the infiltration of IL10-producing Treg cells. We conclude that IKKα is involved in kidney recovery and regeneration through the Treg cells that can produce IL10, which might be a potential therapeutic target that can be used to promote kidney repair after IR injury.

Indexed as

Acute Kidney InjuryAnimalsCell LineCell ProliferationDisease Models, AnimalEpithelial CellsFemaleI-kappa B KinaseIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-10Kidney TubulesMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicChuk protein, mouseI-kappa B KinaseIL10 protein, mouseIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-10NF-kappa B3-dioxygenaseIL10Indoleamine 2Ischemia-reperfusion injuryIκB kinase αKidneyRepairT regular cell

Identifiers

PMID26035380
PMCPMC4486855
OpenAlexW2139650585

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.