Evidence map›Paper›PMID 29057462›Full record

ArticleBritish journal of pharmacology2018

Insulin-like growth factor-1 activates PI3K/Akt signalling to protect human retinal pigment epithelial cells from amiodarone-induced oxidative injury.

Rifang Liao, Fengxia Yan, Zhuanping Zeng, Haitao Wang, Kaifeng Qiu, Jinying Xu, Wenhua Zheng

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  13. [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

7 authors at 3 institutions in 2 countries.

Rifang LiaoFaculty of Health Sciences, University of Macau, Taipa, Macau, and UM Zhuhai Research Institute, Zhuhai, China.
Fengxia YanFaculty of Health Sciences, University of Macau, Taipa, Macau, and UM Zhuhai Research Institute, Zhuhai, China.
Zhuanping ZengSchool of Public Health, Guangdong Pharmaceutical University, Guangzhou, China.
Haitao WangFaculty of Health Sciences, University of Macau, Taipa, Macau, and UM Zhuhai Research Institute, Zhuhai, China.
Kaifeng QiuDepartment of Pharmacy, Sun Yat-Sen Memorial Hospital and the School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Jinying XuFaculty of Health Sciences, University of Macau, Taipa, Macau, and UM Zhuhai Research Institute, Zhuhai, China.
Wenhua ZhengFaculty of Health Sciences, University of Macau, Taipa, Macau, and UM Zhuhai Research Institute, Zhuhai, China.ORCID 0000-0002-3293-3070
Sun Yat-sen University · CNUniversity of Macau · MOGuangdong Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAmiodarone is one of the most effective anti-arrhythmic drugs available, but its clinical applications are limited by toxic side effects including optic toxicity. The purpose of this study was to investigate the toxic effect of amiodarone on D407 cells (a human retinal pigmented epithelial (RPE) cell line) and the mechanisms of the protective effect of insulin-like growth factor-1 (IGF-1). EXPERIMENTAL APPROACH: The involvement of the kinases, Akt and ERK, was analysed by Western blot. Intracellular accumulation of ROS was measured using fluorophotometric quantification. A pharmacological approach with inhibitors was used to investigate the pathways involved in the protective action of IGF-1. KEY

resultsAmiodarone concentration-dependently augmented the production of ROS, lipid peroxidation and apoptosis in D407 cells. IGF-1 time- and concentration-dependently reversed these effects of amiodarone and protected D407 cells from amiodarone-mediated toxicity. Amiodarone inhibited the pAkt but not pErk, and IGF-1 reversed this inhibitory effect of amiodarone. However, IGF-1 failed to suppress amiodarone-induced cytotoxicity in the presence of PI3K/Akt inhibitor LY294002 suggesting the direct involvement of the PI3K/Akt pathway. Furthermore, in vivo rat flash electroretinogram (FERG) recordings showed that IGF-1 reverses the amiodarone-induced decrease in a- and b-waves. The immunocytochemistry findings confirmed that vitreous IGF-1 injections promote the survival of RPE cells in rat retina treated with amiodarone. CONCLUSION AND IMPLICATIONS: IGF-1 can protect RPE cells from amiodarone-mediated injury via the PI3K/Akt pathway in vivo and in vitro. IGF-1 has potential as a protective drug for the prevention and treatment of amiodarone-induced optic toxicity.

Indexed as

AmiodaroneAnimalsCell LineCell SurvivalCytoprotectionDose-Response Relationship, DrugFemaleHumansInsulin-Like Growth Factor IMaleOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyRetinal Pigment EpitheliumAmiodaroneIGF1 protein, humanInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID29057462
PMCPMC5740246
OpenAlexW2766310642

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.