Evidence map›Paper›PMID 37466884›Full record

ArticleApplied biochemistry and biotechnology2024

An In Silico Investigation of Pharmacological Modulators and Inflammasomes in Glioblastoma Multiforme.

Roohi Parveen, Mohd Kashif, Hemalatha Srinivasan, Jasim Khan, Amar Yousif, Dina Saeed Ghataty, Nemat Ali, Sabry M Attia, Mohammad Waseem

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In one paragraph

Article in Applied biochemistry and biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Targeting JNK3: AnCNS & neurological disorders drug targets · 2026
    Article
  2. 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

9 authors at 5 institutions in 4 countries.

Roohi ParveenSchool of Life Sciences, B.S. Abdur Rahman Crescent Institute of Science and Technology, Chennai, 600048, India.
Mohd KashifSchool of Life Sciences, B.S. Abdur Rahman Crescent Institute of Science and Technology, Chennai, 600048, India.
Hemalatha SrinivasanSchool of Life Sciences, B.S. Abdur Rahman Crescent Institute of Science and Technology, Chennai, 600048, India.
Jasim KhanUAB Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
Amar YousifSchool of Pharmacy and Health Professions, University of Maryland Eastern Shore, Princess Anne, MD, USA.
Dina Saeed GhatatyDepartment of Pharmaceutics, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), Giza, Egypt.
Nemat AliDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Saudi Arabia.
Sabry M AttiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Saudi Arabia.
Mohammad WaseemSchool of Life Sciences, B.S. Abdur Rahman Crescent Institute of Science and Technology, Chennai, 600048, India. mohd.waseem193@gmail.com.ORCID http://orcid.org/0000-0002-1708-0137
B.S. Abdur Rahman Crescent Institute of Science & Technology · INKing Saud University · SAOctober University of Modern Sciences and Arts · EGUniversity of Alabama at Birmingham · USUniversity of Maryland Eastern Shore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For the past decades, inflammatory signals have been considered a possible key for pharmacological interventions. There are several compounds and/or molecules that have been known as most promising medication against inflammation and its mediated chronic disorders. Inflammasomes could be recognized as a trigger by detrimental stimuli as pathogenic attack and endogenous signals mediated injury inside the cells. In addition, there has been an inflammatory key mechanism involved in cancers including glioblastoma multiforme (GBM). GBM has been considered the foremost aggressive primary brain tumors in adult stage. There is a scattered beam of light on both cellular and molecular links in inflammation and GBM. However, the immune response of GBM has been characterized extensively by macrophages and lymphocytes related to tumors, and some recent investigations have pinpointed the focus of inflammasomes on the progression of GBM. Nevertheless, risk factors linked with GBM are still debatable. In our study, the most considerable compounds and their bonded and/or targeted proteins have depicted the most promising highlights under in silico condition. Our in silico investigations have revealed a powerful pharmacological agents/compound against inflammasome-mediated GBM.

Indexed as

GlioblastomaInflammasomesBrain NeoplasmsComputer SimulationHumansMolecular Docking SimulationInflammasomesGlioblastoma multiforme Molecular dockingInflammasomesIn silicoPharmacological inhibitor

Identifiers

PMID37466884
OpenAlexW4384665311

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.