Evidence map›Paper›PMID 29085977›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2018

All-trans-retinoic acid ameliorates doxorubicin-induced cardiotoxicity: in vivo potential involvement of oxidative stress, inflammation, and apoptosis via caspase-3 and p53 down-expression.

Asmaa F Khafaga, Yasser S El-Sayed

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2018. 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
4.3field-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

24 citing papers in PubMed, 64 citations in OpenAlex.

  1. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
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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

2 authors at 2 institutions in 1 country.

Asmaa F KhafagaDepartment of Pathology, Faculty of Veterinary Medicine, Alexandria University, Edfina, 22758, Egypt.
Yasser S El-SayedDepartment of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, Egypt. elsayed-ys@vetmed.dmu.edu.eg.
Alexandria University · EGDamanhour University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the potential protective effect of all-trans-retinoic acid (ATRA, a natural derivative of vitamin A) against doxorubicin (DOX)-induced in vivo cardiac toxicity and its underlying mechanisms. Forty male albino rats were allocated into control, ATRA (0.5 mg/kg bwt, intraperitoneally daily), DOX (2.5 mg/kg bwt, intraperitoneally twice weekly for 3 weeks), and DOX + ATRA groups. Serum lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase-cardiac type (CK-MB), troponin I, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were measured. In addition, cardiac glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT), and malondialdehyde (MDA) were determined. Cardiac tissues were examined for histopathologic changes and immunoexpression of pro-apoptotic caspase 3 and tumor-suppressor p53 proteins. DOX caused severe myocardial damage; degenerative and necrotic changes and worsened cardiac function biomarkers; and elevated serum LDH, CK, CK-MB, and troponin I. In addition, DOX inhibited cardiac antioxidative enzymes (GSH, GSH-Px, SOD, CAT) activities and enhanced MDA level. DOX increased serum proinflammatory cytokines (TNF-α, IL-6) and area percent of caspase 3 and p53 immunoexpression in heart tissues. Pretreatment with ATRA maintained cardiac function biomarkers, and reduced proinflammatory cytokines, lipid peroxidation, and immunoexpression of caspase 3 and p53. Moreover, ATRA improved cardiac histoarchitecture, as well as the activities of antioxidative enzymes. Collectively, ATRA can counteract DOX-induced cardiomyopathy through antioxidative and anti-inflammatory properties, besides suppression of the activation of the mitochondrial apoptotic pathway.

Indexed as

AnimalsApoptosisCardiotoxicityCaspase 3Down-RegulationDoxorubicinGenes, p53InflammationMaleMyocardiumOxidative StressRatsRats, WistarTretinoinCaspase 3DoxorubicinTretinoinAll-trans-retinoic acidApoptosisCardiotoxicityCytokinesImmunohistochemistryOxidative stress

Identifiers

PMID29085977
OpenAlexW2765855314

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.