Evidence map›Paper›PMID 27774572›Full record

ArticleMolecular neurobiology2017

Amiodarone-Induced Retinal Neuronal Cell Apoptosis Attenuated by IGF-1 via Counter Regulation of the PI3k/Akt/FoxO3a Pathway.

Rifang Liao, Fengxia Yan, Zhuanping Zeng, Mohd Farhan, Peter Little, Remi Quirion, Lalit K Srivastava, Wenhua Zheng

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

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  12. [Amiodarone promotes heat-induced apoptosis, inflammation and oxidative stress in mouse HL1 atrial myocytes].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
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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

8 authors at 6 institutions in 4 countries.

Rifang LiaoNeuropharmacology, School of Pharmaceutical Sciences, and Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Fengxia YanNeuropharmacology, School of Pharmaceutical Sciences, and Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Zhuanping ZengSchool of Public Health, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
Mohd FarhanFaculty of Health Sciences, University of Macau, Room 4021, Building E12, Avenida de Universidade, Taipa, Macau, China.
Peter LittleSchool of Pharmacy, Pharmacy Australia Centre of Excellence (PACE), The University of Queensland, 20 Cornwall St, Woolloongabba, QLD, 4102, Australia.
Remi QuirionDouglas Hospital Research Center, McGill University, Montreal, QC, Canada.
Lalit K SrivastavaDouglas Hospital Research Center, McGill University, Montreal, QC, Canada.
Wenhua ZhengNeuropharmacology, School of Pharmaceutical Sciences, and Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China. wenhuazheng@umac.mo.
University of Macau · MODouglas Mental Health University Institute · CAGuangdong Pharmaceutical University · CNMcGill University · CASun Yat-sen University · CNUniversity of Queensland · AU

Funding

National Natural Science Fund of China No 31371088
6 · The paper itself

Abstract

Amiodarone (AM) is the most effective antiarrhythmic agent currently available. However, clinical application of AM is limited by its serious toxic adverse effects including optic neuropathy. The purpose of this study was to explore the effects of AM and to assess if insulin-like growth factor-1 (IGF-1) could protect retinal neuronal cells from AM-induced apoptosis, and to determine the molecular mechanisms underlying the effects. Accordingly, the phosphorylation/activation of Akt and FoxO3a were analyzed by Western blot while the possible pathways involved in the protection of IGF-1 were investigated by application of various pathway inhibitors. The full electroretinogram (FERG) was used to evaluate in vivo effect of AM and IGF-1 on rat retinal physiological functions. Our results showed that AM concentration dependently caused an apoptosis of RGC-5 cells, while IGF-1 protected RGC-5 cells against this effect by AM. The protective effect of IGF-1 was reversed by PI3K inhibitors LY294002 and wortmannin as well as the Akt inhibitor VIII. AM decreased p-Akt and p-FoxO3a while increased the nuclear localization of FoxO3a in the RGC-5 cells. IGF-1 reversed the effect of AM on the p-Akt and p-FoxO3a and the nuclear translocation of FoxO3a. Similar results were obtained in primary cultured retinal ganglia cells. Furthermore, FERG in vivo recording in rats showed that AM decreased a-wave and b-wave of FERG while IGF-1 reversed the effects of AM. These data show that AM induced apoptosis of retinal neuronal cells via inhibiting the PI3K/Akt/FoxO3a pathway while IGF-1 protected RGC-5 cells against AM-induced cell apoptosis by stimulating this pathway.

Indexed as

ApoptosisSignal TransductionAmiodaroneAnimalsAnimals, NewbornCell LineChromonesElectroretinographyForkhead Box Protein O3Insulin-Like Growth Factor IModels, BiologicalMorpholinesPhosphatidylinositol 3-KinasesPhosphorylationProtective AgentsProtein Kinase Inhibitors2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAmiodaroneChromonesForkhead Box Protein O3FOXO3 protein, ratInsulin-Like Growth Factor IMorpholinesPhosphatidylinositol 3-KinasesProtective AgentsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktAktAmiodaroneAntiarrhythmicApoptosisFoxO3aNeuroprotection

Identifiers

PMID27774572
OpenAlexW2536334800

What OpenQuestion holds

Textmetadata
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.