Evidence map›Paper›PMID 24407718›Full record

ArticleMedical molecular morphology2014

Renal atrophy after ischemia-reperfusion injury depends on massive tubular apoptosis induced by TNFα in the later phase.

Takaomi Adachi, Noriyuki Sugiyama, Hideo Yagita, Takahiko Yokoyama

Abstract read
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In one paragraph

Article in Medical molecular morphology, 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
2.3field-weighted citation impact, top 13% 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, 30 citations in OpenAlex.

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  11. Food strategies of renal atrophy based on Avicenna and conventional medicine.Journal of traditional and complementary medicine · 2017
    Review
  12. Effects of sevoflurane on NF-кB and TNF-α expression in renal ischemia-reperfusion diabetic rats.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Kidney-specific Sonoporation-mediated Gene Transfer.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    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 1 country.

Takaomi AdachiDepartment of Anatomy and Developmental Biology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Noriyuki Sugiyama
Hideo Yagita
Takahiko Yokoyama
Kyoto Prefectural University of Medicine · JPJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have suggested that acute kidney injury (AKI) develops into chronic kidney disease (CKD). However, a mechanism for disease progression from AKI to CKD has not been established. We developed two ischemia-reperfusion injury (IRI) mouse models, a repaired kidney model and an atrophic kidney model, and studied the mechanisms of renal atrophy after IRI by comparing the two models. We found that renal atrophy after IRI depended on tubular apoptosis at 14 days after IRI. Moreover, we found that Tnfα and FasL mRNA were synchronously expressed at the time of tubular apoptosis. To elucidate the relationship between tubular apoptosis and apoptotic ligands, we administered TNFα and FasL neutralizing antibodies according to the time of tubular apoptosis. TNFα blockade significantly repressed tubular apoptosis, resulting in the prevention of renal atrophy. FasL blockade could not repress tubular apoptosis, resulting in renal atrophy. We also found that TNF receptors were expressed in the kidney at 14 days after IRI, but Fas receptor was not. We concluded that renal atrophy after IRI depends on tubular apoptosis induced by the TNFα signaling pathway in the later phase of renal IRI, and that TNFα blockade could be a potential new therapeutic approach for improving renal prognosis after AKI.

Indexed as

ApoptosisAnimalsAtrophyFas Ligand Proteinfas ReceptorIschemiaKidney TubulesMaleMiceReceptors, Tumor Necrosis FactorReperfusion InjurySignal TransductionTumor Necrosis Factor-alphaUp-RegulationFas Ligand Proteinfas ReceptorReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID24407718
OpenAlexW1993470854

What OpenQuestion holds

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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.