Evidence map›Paper›PMID 38077444›Full record

ArticlePeerJ2023

Pharmacoscreening, molecular dynamics, and quantum mechanics of inermin from

Janakiraman V, Sudhan M, Abubakar Wani, Sheikh F Ahmad, Ahmed Nadeem, Ashutosh Sharma, Shiek S S J Ahmed

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2023. 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
0.5field-weighted citation impact, top 32% 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, 3 citations in OpenAlex.

  1. Article
  2. Phytoconstituents ofACS omega · 2025
    Article
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 4 institutions in 4 countries.

Janakiraman VMuti-omics and Drug Discovery Lab, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettnad Academy of Research and Education, Kelambakkam, Tamil Nadu, India.
Sudhan MMuti-omics and Drug Discovery Lab, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettnad Academy of Research and Education, Kelambakkam, Tamil Nadu, India.
Abubakar WaniDepartment of Immunology, St. Jude Children's Research Hospital Memphis, TN, USA.
Sheikh F AhmadDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Ahmed NadeemDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Ashutosh SharmaCentre of Bioengineering, NatProLab, Plant Innovation Lab, School of Engineering and Sciences, Tecnologico de Monterrey, Queretaro, Mexico.
Shiek S S J AhmedMuti-omics and Drug Discovery Lab, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettnad Academy of Research and Education, Kelambakkam, Tamil Nadu, India.
Chettinad Academy of Research and Education · INKing Saud University · SASt. Jude Children's Research Hospital · USTecnológico de Monterrey · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Exosomes, microvesicles, carry and release several vital molecules across cells, tissues, and organs. Epicardial adipose tissue exosomes are critical in the development and progression of coronary artery disease (CAD). It is hypothesized that exosomes may transport causative molecules from inflamed tissue and deliver to the target tissue and progress CAD. Thus, identifying and inhibiting the CAD-associated proteins that are being transported to other cells via exosomes will help slow the progression of CAD. Methods: This study uses a systems biological approach that integrates differential gene expression in the CAD, exosomal cargo assessment, protein network construction, and functional enrichment to identify the crucial exosomal cargo protein target. Meanwhile, absorption, distribution, metabolism, and excretion (ADME) screening of Results: Through the systems biological approach, Mothers against decapentaplegic homolog 2 protein (SMAD2) was determined as a potential target that linked with PI3K-Akt signaling, Ubiquitin mediated proteolysis, and the focal adhesion pathway. Further, screening of 190

Indexed as

Coronary Artery DiseasePanaxLigandsMolecular Dynamics SimulationPhosphatidylinositol 3-KinasesPhytoalexinsPterocarpansinerminLigandsPhosphatidylinositol 3-KinasesPhytoalexinsPterocarpansCoronary artery diseaseDensity functional theoryExosomesMolecular dynamic simulationProtein networkSystems biology

Identifiers

PMID38077444
PMCPMC10710165
OpenAlexW4389391617

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.