Evidence map›Paper›PMID 24915841›Full record

ArticleAging cell2014

Bmi-1 plays a critical role in protection from renal tubulointerstitial injury by maintaining redox balance.

Jianliang Jin, Xianhui Lv, Lulu Chen, Wei Zhang, Jinbo Li, Qian Wang, Rong Wang, Xiang Lu, Dengshun Miao

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. p16Journal of cardiovascular translational research · 2025
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  3. Retraction Note: P16Scientific reports · 2025
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  10. Review
  11. P16Frontiers in cell and developmental biology · 2021
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  14. Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020
    Review
  15. Prevention of tumor risk associated with the reprogramming of human pluripotent stem cells.Journal of experimental & clinical cancer research : CR · 2020
    Review
  16. Article
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  18. Article
  19. Article
  20. P16American journal of translational research · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Jianliang JinThe State Key Laboratory of Reproductive Medicine, Department of Anatomy, Histology and Embryology, Nanjing Medical University, Nanjing, China.
Xianhui Lv
Lulu Chen
Wei Zhang
Jinbo Li
Qian Wang
Rong Wang
Xiang Lu
Dengshun Miao
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To determine whether Bmi-1 deficiency could lead to renal tubulointerstitial injury by mitochondrial dysfunction and increased oxidative stress in the kidney, 3-week-old Bmi-1(-/-) mice were treated with the antioxidant N-acetylcysteine (NAC, 1 mg mL(-1) ) in their drinking water, or pyrro-quinoline quinone (PQQ, 4 mg kg(-1) diet) in their diet for 2 weeks, and their renal phenotypes were compared with vehicle-treated Bmi1(-/-) and wild-type mice. Bmi-1 was knocked down in human renal proximal tubular epithelial (HK2) cells which were treated with 1 mm NAC for 72 or 96 h, and their phenotypes were compared with control cells. Five-week-old vehicle-treated Bmi-1(-/-) mice displayed renal interstitial fibrosis, tubular atrophy, and severe renal function impairment with decreased renal cell proliferation, increased renal cell apoptosis and senescence, and inflammatory cell infiltration. Impaired mitochondrial structure, decreased mitochondrial numbers, and increased oxidative stress occurred in Bmi-1(-/-) mice; subsequently, this caused DNA damage, the activation of TGF-β1/Smad signaling, and the imbalance between extracellular matrix synthesis and degradation. Oxidative stress-induced epithelial-to-mesenchymal transition of renal tubular epithelial cells was enhanced in Bmi-1 knocked down HK2 cells. All phenotypic alterations caused by Bmi-1 deficiency were ameliorated by antioxidant treatment. These findings indicate that Bmi-1 plays a critical role in protection from renal tubulointerstitial injury by maintaining redox balance and will be a novel therapeutic target for preventing renal tubulointerstitial injury.

Indexed as

AnimalsCell Line, TumorDNA DamageEpithelial-Mesenchymal TransitionGenotyping TechniquesHumansKidneyKidney DiseasesMitogen-Activated Protein Kinase 7Nephritis, InterstitialOxidation-ReductionOxidative StressMAPK7 protein, humanMitogen-Activated Protein Kinase 7antioxidantBmi-1DNA damageepithelial-to-mesenchymal transitionoxidative stressrenal tubulointerstitial injury

Identifiers

PMID24915841
PMCPMC4331754
OpenAlexW2127156190

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.