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Activation of AMPK/mTOR-Driven Autophagy and Suppression of the HMGB1/TLR4 Pathway with Pentoxifylline Attenuates Doxorubicin-Induced Hepatic Injury in Rats

Pharmaceuticals(2024)10.3390/ph17060681Source: DataRank Database

Activation of AMPK/mTOR-Driven Autophagy and Suppression of the HMGB1/TLR4 Pathway with Pentoxifylline Attenuates Doxorubicin-Induced Hepatic Injury in Rats is a research paper published in Pharmaceuticals (2024). On theSindex it has a DataRank of 0. It has been cited 11 times.

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0DataRank · unranked

Scored on demand from live citation data

Open Access11 citations

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›Methodology & internals

datarank_citation_only_1hop_v6· scope data_onlyMethodology

Pipeline:MetadataData-paper checkEnrichmentCitation networkScoring

Enrichment:Funding (1 grants)Impact (FWCI 3.44)OA: goldTopics (22)IDs (PubMed, PMC, OpenAlex)SDGs (1)

FAIR Checklist

Context only (not used in score)

Findable (1/2)

Has DOI

Accessible (1/2)

Open Access

Interoperable (0/2)

Reusable (0/3)

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Authors (13)

Ahmed H. Eid,Shuruq E. Alsufyani ORCID,Ahmed M. Ashour ORCID,Alwaleed M. Alnefaie,Nasser Al-Sharif ORCID

Live enrichment

PubMed:38931349 PMC:PMC11206793 OpenAlex:https://openalex.org/W4399042672

Taif University

Grant: TU-DSPP-2024-116

FWCI

3.44

Citation Percentile

0.9%

Citation Trend

2025

2026

goldLicense: cc-by

journalhttps://www.mdpi.com/1424-8247/17/6/681/pdf?version=1716858957

publisherhttps://www.mdpi.com/1424-8247/17/6/681/pdf?version=1716858957

publisherhttps://www.mdpi.com/1424-8247/17/6/681/pdf

journalhttps://doi.org/10.3390/ph17060681

repositoryhttps://pubmed.ncbi.nlm.nih.gov/38931349

Fields of Study

Autophagy in Disease and TherapyChemotherapy-induced cardiotoxicity and mitigationCell death mechanisms and regulation

Keywords

AutophagyHMGB1PentoxifyllineAMPKPI3K/AKT/mTOR pathwayTLR4PharmacologyMedicineInflammationDoxorubicinApoptosisLiver injuryCancer researchChemistryInternal medicineChemotherapyProtein kinase ABiochemistryHepatotoxicity

Sustainable Development Goals

SDG 0: Good health and well-being