Evidence map›Paper›PMID 36197604›Full record

ArticleMolecular diagnosis & therapy2022

Functional Association of miR-133b and miR-21 Through Novel Gene Targets ATG5, LRP6 and SGPP1 in Coronary Artery Disease.

Dinesh Kumar, Rajiv Narang, Daman Saluja, Kamna Srivastava

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Article in Molecular diagnosis & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Dinesh KumarDr. B R Ambedkar Center for Biomedical Research, University of Delhi, New Delhi, 110007, India.
Rajiv NarangDepartment of Cardiology, All India Institute of Medical Sciences, New Delhi, 110029, India.
Daman SalujaDr. B R Ambedkar Center for Biomedical Research, University of Delhi, New Delhi, 110007, India.
Kamna SrivastavaDr. B R Ambedkar Center for Biomedical Research, University of Delhi, New Delhi, 110007, India. Kamna605@gmail.com.
University of Delhi · INAll India Institute of Medical Sciences · INAmbedkar University Delhi · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis, a progressive manifestation of coronary artery disease, has been observed to be regulated by microRNAs (miRNAs) targeting various protein-coding genes involved in several pathophysiological events of coronary artery disease.

objectiveIn our previous report, we identified differential expression profiles of candidate miRNAs, miR-133b and miR-21, in patients with coronary artery disease as compared with controls, suggesting their possible implication in the pathophysiology of coronary artery disease. To better understand the functional role of these miRNAs, we sought to predict and validate their target genes while assessing the expression pattern of these genes in patients with coronary artery disease, as well as in macrophages.

methodsPotential target genes of miR-133b and miR-21 were predicted bioinformatically followed by validation through the identification of their expression at  the protein level in patients with coronary artery disease (n-30), as well as in macrophages treated with respective miRNA inhibitors (antagomiRs), through immunoblotting.

resultsSGPP1, a gene associated with the sphingolipid pathway, was predicted to be a potential target gene of miR-133b while ATG5 and LRP6 were target genes of miR-21 while being associated with autophagy and Wnt signalling pathways, respectively. SGPP1 was observed to be upregulated significantly (p = 0.019) by 2.07-fold, whereas ATG5 and LRP6 were found to be downregulated (p = 0.026 and 0.007, respectively) by 3.28-fold and 8.46-fold, respectively, in patients with coronary artery disease as compared with controls. Expression patterns of all the genes were also found to be modulated when cells were treated with respective miRNA inhibitors.

conclusionsResults from the present study suggest that SGPP1, ATG5 and LRP6, target genes of miR-133b and miR-21, may serve as potential therapeutic hotspots in the management of coronary artery disease, which undoubtedly merit further experimental confirmation.

Indexed as

Coronary Artery DiseaseMicroRNAsAutophagy-Related Protein 5HumansLow Density Lipoprotein Receptor-Related Protein-6Membrane ProteinsPhosphoric Monoester HydrolasesATG5 protein, humanAutophagy-Related Protein 5Low Density Lipoprotein Receptor-Related Protein-6LRP6 protein, humanMembrane ProteinsMicroRNAsMIRN21 microRNA, humanPhosphoric Monoester HydrolasesSGPP1 protein, human

Identifiers

PMID36197604
OpenAlexW4301401196

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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.