Evidence map›Paper›PMID 24884644›Full record

ArticleBMC neuroscience2014

Calpain: a molecule to induce AIF-mediated necroptosis in RGC-5 following elevated hydrostatic pressure.

Lei Shang, Ju-Fang Huang, Wei Ding, Shuang Chen, Li-Xiang Xue, Ruo-Fei Ma, Kun Xiong

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 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
2.7field-weighted citation impact, top 10% 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, 44 citations in OpenAlex.

  1. Genetic and Epigenetic Factors in Gestational Diabetes Mellitus Pathology.International journal of molecular sciences · 2023
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  8. A lab-on-a-chip model of glaucoma.Brain and behavior · 2020
    Article
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  13. Regulatory role of calpain in neuronal death.Neural regeneration research · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Inhibition of calpain on oxygen glucose deprivation-induced RGC-5 necroptosis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016
    Article
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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

7 authors at 2 institutions in 1 country.

Lei Shang
Ju-Fang Huang
Wei Ding
Shuang Chen
Li-Xiang Xue
Ruo-Fei Ma
Kun XiongDepartment of Anatomy and Neurobiology, Central South University School of Basic Medical Sciences, 172 Tongzi Po Road, 410013 Changsha, Hunan, China. xiongkun2001@163.com.
Central South University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRIP3 (Receptor-interacting protein 3) pathway was mainly described as the molecular mechanism of necroptosis (programmed necrosis). But recently, non-RIP3 pathways were found to mediate necroptosis. We deliberate to investigate the effect of calpain, a molecule to induce necroptosis as reported (Cell Death Differ 19:245-256, 2012), in RGC-5 following elevated hydrostatic pressure.

resultsFirst, we identified the existence of necroptosis of RGC-5 after insult by using necrostatin-1 (Nec-1, necroptosis inhibitor) detected by flow cytometry. Immunofluorescence staining and western blot were used to detect the expression of calpain. Western blot analysis was carried out to describe the truncated AIF (tAIF) expression with or without pretreatment of ALLN (calpain activity inhibitor). Following elevated hydrostatic pressure, necroptotic cells pretreated with or without ALLN was stained by Annexin V/PI, The activity of calpain was also examined to confirm the inhibition effect of ALLN. The results showed that after cell injury there was an upregulation of calpain expression. Upon adding ALLN, the calpain activity was inhibited, and tAIF production was reduced upon injury along with the decreased number of necroptosis cells.

conclusionOur study found that calpain may induce necroptosis via tAIF-modulation in RGC-5 following elevated hydrostatic pressure.

Indexed as

Mechanotransduction, CellularApoptosisApoptosis Inducing FactorCalpainCell LineHumansHydrostatic PressureNecrosisRetinal Ganglion CellsAIFM1 protein, mouseApoptosis Inducing FactorCalpain

Identifiers

PMID24884644
PMCPMC4023497
OpenAlexW2027371168

What OpenQuestion holds

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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.