Evidence map›Paper›PMID 34194837›Full record

ArticleJournal of advanced research2021

Dabigatran mitigates cisplatin-mediated nephrotoxicity through down regulation of thrombin pathway.

Mohamed Gamal El-Din Ewees, Mohamed Sadek Abdel-Bakky, Asmaa Mostafa Ahmed Bayoumi, Ali Ahmed Abo-Saif, Waleed Mohammad Altowayan, Khalid Saad Alharbi, Basim Anwar Shehata Messiha

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Ferroptosis: A Potential Therapeutic Target in Acute Kidney Injury.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Nephrotoxicity in cancer treatment: An update.Advances in cancer research · 2022
    Article
  10. Folic acid-induced animal model of kidney disease.Animal models and experimental medicine · 2021
    Review
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 6 institutions in 2 countries.

Mohamed Gamal El-Din EweesDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Nahda University, Beni-Suef, Egypt.
Mohamed Sadek Abdel-BakkyDepartment of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Qassim, Saudi Arabia.
Asmaa Mostafa Ahmed BayoumiDepartment of Biochemistry, Faculty of Pharmacy, Minia University, Minia, Egypt.
Ali Ahmed Abo-SaifDepartment of Pharmacology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
Waleed Mohammad AltowayanDepartment of Pharmacy Practice, College of Pharmacy, Qassim University, Qassim, Saudi Arabia.
Khalid Saad AlharbiDepartment of Pharmacology, College of Pharmacy, Jouf University, Sakakah, Saudi Arabia.
Basim Anwar Shehata MessihaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt.
Al-Azhar University · EGAl Jouf University · SABeni-Suef University · EGMinia University · EGNahda University · EGQassim University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCisplatin (CDDP) nephrotoxicity is one of the most significant complications limiting its use in cancer therapy.

objectivesThis study investigated the pivotal role played by thrombin in CDDP-mediated nephrotoxicity. This work also aimed to clarify the possible preventive effect of Dabigatran (Dab), a direct thrombin inhibitor, on CDDP nephrotoxicity.

methodsAnimals were grouped as follow; normal control group, CDDP nephrotoxicity group, CDDP + Dab 15, and CDDP + Dab 25 groups. Four days following CDDP administration, blood and urine samples were collected to evaluate renal function. Moreover, tissue samples were collected from the kidney to determine apoptosis markers, oxidative stress and histopathological evaluation. An immunofluorescence analysis of tissue factor (TF), thrombin, protease-activated receptor-2 (PAR2), fibrin, pERK1/2 and P53 proteins expression was also performed.

resultsThrombin, pERK, cleaved caspase-3, and oxidative stress markers were significantly elevated in CDDP-treated group. However, pretreatment of animals with either low or high doses of Dab significantly improved kidney function and decreased oxidative stress and apoptotic markers.

conclusionWe conclude that thrombin is an important factor in the pathogenesis of CDDP kidney toxicity via activation of ERK1/2, P53 and caspase-3 pathway, which can be effectively blocked by Dab.

Indexed as

AnimalsAntithrombinsApoptosisBlood Urea NitrogenCaspase 3CisplatinDabigatranDown-RegulationKidneyKidney DiseasesMaleMAP Kinase Signaling SystemNeoplasmsOxidative StressRatsThrombinAntithrombinsCaspase 3CisplatinDabigatranThrombinTumor Suppressor Protein p53BUN, Blood urea nitrogenCDDP, CisplatinCisplatinCrcl, Creatinine cleranceCr, creatinineDab, DabigatranDabigatranFXa, activated form of Factor XGSH, Reduced GlutathionH&E, Hematoxylin–EosinINR, International normalized ratioKIM-1, kidney injury molecule-1PAR2PAR, protease-activated receptorpERK1/2Pt, Prothrombin timePtt, Partial thromboplastin timeROS, Reactive oxygen speciesSOD, Superoxide dismutaseTF, Tissue factorThrombin

Identifiers

PMID34194837
PMCPMC8240102
OpenAlexW3120357487

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.