Evidence map›Paper›PMID 34185243›Full record

ArticleCardiovascular drugs and therapy2022

The IL-6/STAT Signaling Pathway and PPARα Are Involved in Mediating the Dose-Dependent Cardioprotective Effects of Fenofibrate in 5-Fluorouracil-Induced Cardiotoxicity.

Marwa M M Refaie, Sayed Shehata, Asmaa M A Bayoumi, Nashwa Fathy Gamal El-Tahawy, Walaa Yehia Abdelzaher

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Article in Cardiovascular drugs and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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  10. Antioxidant and anti-inflammatory activities of lycopene against 5-fluorouracil-induced cytotoxicity in Caco2 cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    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

5 authors at 2 institutions in 2 countries.

Marwa M M RefaieDepartment of Pharmacology, Faculty of Medicine, Minia University, El-Minia, 61511, Egypt. marwamonier@yahoo.com.ORCID 0000-0001-6211-9558
Sayed ShehataDepartment of Cardiology, Faculty of Medicine, Minia University, El-Minia, 61511, Egypt.
Asmaa M A BayoumiDepartment of Biochemistry, Faculty of Pharmacy, Minia University, El-Minia, 61511, Egypt.
Nashwa Fathy Gamal El-TahawyDepartment of Histology and Cell biology, Faculty of Medicine, Minia University, El-Minia, 61511, Egypt.
Walaa Yehia AbdelzaherDepartment of Pharmacology, Faculty of Medicine, Minia University, El-Minia, 61511, Egypt.
Minia University · EGKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe cardiotoxicity of anticancer drugs such as 5-fluorouracil (5FU) is a major complication that challenges their clinical usefulness. Thus there is a critical need to find new protective drugs to defend against these harmful side effects. Up to now, there have been no studies evaluating the possible cardioprotective effects of fenofibrate (FEN) in 5FU-induced cardiotoxicity. Therefore, we aimed in the current model to evaluate such an effect of FEN and to explore different mechanisms mediating it.

methodsWe used FEN (25, 50, 100 mg/kg/day) administered orally for 7 days with induction of cardiotoxicity by intraperitoneal (i.p.) injection of 5FU (150 mg/kg) on the fifth day.

resultsThe current study showed that 5FU succeeded in inducing cardiotoxicity, manifested by significantly elevated levels of cardiac enzymes, tissue malondialdehyde (MDA), interleukin 6 (IL-6), signal transducer and activator of transcription 4 (STAT4), and caspase-3. Furthermore, the 5FU group showed toxic histopathological changes including marked cardiac damage and a significant decrease in reduced glutathione (GSH), total antioxidant capacity (TAC), and peroxisome proliferator-activated receptor alpha (PPARα) expression. FEN reversed 5FU-induced cardiotoxicity by various mechanisms including upregulation of PPARα, inhibition of the IL-6/STAT signaling pathway, and anti-inflammatory, antiapoptotic, and antioxidant properties.

conclusionFEN demonstrated a significant cardioprotective effect against 5FU-induced cardiac damage.

Indexed as

FenofibratePPAR alphaAntioxidantsCardiotoxicityCaspase 3FluorouracilGlutathioneHumansInterleukin-6MalondialdehydeOxidative StressSignal TransductionSTAT4 Transcription FactorAntioxidantsCaspase 3FenofibrateFluorouracilGlutathioneInterleukin-6MalondialdehydePPAR alphaSTAT4 Transcription Factor5-FluorouracilCardiotoxicityFenofibrateInterleukin 6

Identifiers

PMID34185243
OpenAlexW3156495184

What OpenQuestion holds

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Registered trials

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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.