Evidence map›Paper›PMID 32141012›Full record

ArticleInflammopharmacology2020

Apixaban exhibits anti-arthritic effects by inhibiting activated factor X-mediated JAK2/STAT3 and MAPK phosphorylation pathways.

Omnia Ahmed Mohamed Abd El-Ghafar, Gouda Kamel Helal, Amira M Abo-Youssef

Abstract read
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In one paragraph

Article in Inflammopharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

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  15. Mechanism of miR-218-5p in autophagy, apoptosis and oxidative stress in rheumatoid arthritis synovial fibroblasts is mediated by KLF9 and JAK/STAT3 pathways.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 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

3 authors at 3 institutions in 1 country.

Omnia Ahmed Mohamed Abd El-GhafarPharmacology and Toxicology Department, Faculty of Pharmacy, Nahda University, Kornish Al Nil, Bayad Al Arab, Beni Suef, Egypt. omneaahmed25@yahoo.com.
Gouda Kamel HelalPharmacology and Toxicology Department, Faculty of Pharmacy, Heliopolis University for Sustainable Development, 3 Cairo-Belbeis Desert Rd, Second Al Salam, Cairo, Egypt.
Amira M Abo-YoussefPharmacology and Toxicology Department, Faculty of Pharmacy, Beni-Suef University, Beni Suef, Egypt. amira.abouyousif@pharm.bsu.edu.eg.ORCID http://orcid.org/0000-0001-8419-6095
Beni-Suef University · EGHeliopolis University · EGNahda University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activated factor X (FXa) is strongly linked to various inflammatory events. This study aimed to investigate the effect of FXa on janus kinase2/signal transducers and activators of transcription3 (JAK2/STAT3) and mitogen-activated protein kinase (MAPK) phosphorylation in relation to rheumatoid arthritis (RA). It also extends its scope to explore the possible anti-arthritic effects of apixaban, a selective FXa inhibitor. Rats were allocated into normal control; complete Freund's adjuvant (CFA, 0.4 ml/4 days/12 days); FXa (120 µg/kg/day/3 days) and CFA + FXa groups as well as three treated groups including CFA + apixaban; FXa + apixaban and CFA + FXa + apixaban. Apixaban was administered at a dose of 10 mg/kg/12 h for15 days. By the end of the experimental period, tissue samples were collected for the assessment of phosphorylated (p)-JAK2, STAT3, MAPK, matrixmetalloprotein-1 (MMP-1) and protease-activated receptor 2. Furthermore, Serum interleukin-6 (IL-6), platelet-derived growth factor (PDGF), anti-citrullinated protein antibody (ACPA), 8-hydroxy-2'-deoxyguanosine (8-OHdG), plasma level of FXa and prothrombin time were evaluated. In support, histopathological and macroscopical examinations were performed. FXa activated JAK2, STAT3 and MAPK phosphorylation through activation of PAR 2, PDGF and IL-6 and concomitantly led to a significant elevation in ACPA, MMP-1 and 8-OHdG. Apixaban markedly amended FXa-induced changes. Conclusively, the current study revealed that FXa may have a drastic role in RA progression and pathogenesis at least through stimulation of JAK2/STAT3 and MAPK phosphorylation. Furthermore, apixaban exerted robust arthro-protective effects. These beneficial outcomes could be attributed to its ability to impede JAK2/STAT3 and MAPK activation, as well as to its antioxidant property.

Indexed as

AnimalsAntioxidantsAntirheumatic AgentsArthritis, ExperimentalArthritis, RheumatoidDisease ProgressionFactor XaFactor Xa InhibitorsFemaleJanus Kinase 2MAP Kinase Signaling SystemPhosphorylationPyrazolesPyridonesRatsRats, WistarAntioxidantsAntirheumatic AgentsapixabanFactor XaFactor Xa InhibitorsJak2 protein, ratJanus Kinase 2PyrazolesPyridonesStat3 protein, ratSTAT3 Transcription FactorFxaJAK2/STAT3 pathwayMAPK pathwayRheumatoid arthritis

Identifiers

PMID32141012
OpenAlexW3009083611

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.