Evidence map›Paper›PMID 29891925›Full record

ArticleScientific reports2018

Cadmium-induced apoptosis in neuronal cells is mediated by Fas/FasL-mediated mitochondrial apoptotic signaling pathway.

Yan Yuan, Yajing Zhang, Shiwen Zhao, Jie Chen, Jinlong Yang, Tao Wang, Hui Zou, Yi Wang, Jianhong Gu, Xuezhong Liu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 99 citations in OpenAlex.

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  17. Research Progress of DcR3 in the Diagnosis and Treatment of Sepsis.International journal of molecular sciences · 2023
    Review
  18. Review
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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

12 authors at 1 institution in 1 country.

Yan YuanCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Yajing ZhangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Shiwen ZhaoCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Jie ChenCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Jinlong YangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Tao WangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Hui ZouCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Yi WangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Jianhong GuCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Xuezhong LiuCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Jianchun BianCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China.
Zongping LiuCollege of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People's Republic of China. liuzongping@yzu.edu.cn.
Yangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium (Cd) is a toxic metal capable of damaging brain. Studies have demonstrated that Cd can induce apoptosis in neuronal cells. The CD95/APO-1 (Fas)/Fas Ligand (FasL) signaling pathway is one of the primary apoptosis pathways, but the role and regulatory mechanism of this pathway in neuronal cells remain unclear. Here, we demonstrated the underlying mechanism of the Fas/FasL system involving the mitochondrial apoptotic pathway in neuronal cells. Primary rat cerebral cortical neurons and PC12 cells were exposed to Cd, which significantly activated expression of Fas, FasL, Fas-associated death domain (FADD) and cleaved caspase-8. However, expression of cleaved caspase-8 decreased at 20 µM Cd in primary cerebral cortical neurons. Importantly, Cd-induced apoptotic morphological changes and increase in the apoptosis rate were partially blocked by Z-IETD-FMK, which is a specific inhibitor of caspase-8. Cd-mediated increase of apoptosis rate was inhibited by anti-FasL antibody. Furthermore, our data revealed that Z-IETD-FMK also blocked increase of truncated BH3 interacting domain death agonist (tBID)/BID, decrease of the B-cell lymphoma 2 (Bcl-2)/Bcl-2 associate X protein (Bax) ratio and mitochondrial membrane potential (MMP), release of cytochrome c, as well as cleavage of caspase-9/3 and poly (ADP-ribose) polymerase (PARP) induced by Cd. Taken together, our results demonstrate that the Fas/FasL-mediated mitochondrial apoptotic pathway plays an important role in Cd-induced neuronal apoptosis.

Indexed as

ApoptosisAnimalsCadmiumCaspase 8Cells, CulturedFas-Associated Death Domain ProteinFas Ligand Proteinfas ReceptorMitochondriaNeuronsProteolysisRatsSignal TransductionCadmiumCasp8 protein, ratCaspase 8Fadd protein, ratFas-Associated Death Domain ProteinFaslg protein, ratFas Ligand ProteinFas protein, ratfas Receptor

Identifiers

PMID29891925
PMCPMC5995901
OpenAlexW2806233704

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.