Evidence map›Paper›PMID 37387208›Full record

ArticleCirculation. Genomic and precision medicine2023

Network Preservation Analysis Reveals Dysregulated Metabolic Pathways in Human Vascular Smooth Muscle Cell Phenotypic Switching.

R Noah Perry, Diana Albarracin, Redouane Aherrahrou, Mete Civelek

Open access · hybridAbstract read
In one paragraph

Article in Circulation. Genomic and precision medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

4 authors at 2 institutions in 1 country.

R Noah PerryCenter for Public Health Genomics (R.N.P., R.A., M.C.), University of Virginia, Charlottesville.ORCID 0000-0002-3555-0964
Diana AlbarracinDepartment of Biomedical Engineering (R.N.P., D.A., M.C.), University of Virginia, Charlottesville.
Redouane AherrahrouCenter for Public Health Genomics (R.N.P., R.A., M.C.), University of Virginia, Charlottesville.ORCID 0000-0001-8148-9554
Mete CivelekCenter for Public Health Genomics (R.N.P., R.A., M.C.), University of Virginia, Charlottesville.ORCID 0000-0002-8141-0284
University of Virginia · USUniversity of Virginia Medical Center · US

Funding

BASIC CARDIOVASCULAR RESEARCH TRAINING GRANTT32HL007284 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Brant E Isakson, Gary K Owens · 1985 to 2026
$19.6M
Systems Genetics of Vascular Smooth Muscle PhenotypesR01HL166428 · NHLBI · UNIVERSITY OF VIRGINIA · PI Mete Civelek · 2023 to 2026
$2.4M
The role of nitrogen metabolism in smooth muscle cell phenotypic plasticityF31HL165772 · NHLBI · UNIVERSITY OF VIRGINIA · PI PERRY, ROBERT NOAH · 2022 to 2025
$120k
NHLBI NIH HHS F31 HL165772NHLBI NIH HHS R01 HL166428NHLBI NIH HHS T32 HL007284
6 · The paper itself

Abstract

backgroundVascular smooth muscle cells are key players involved in atherosclerosis, the underlying cause of coronary artery disease. They can play either beneficial or detrimental roles in lesion pathogenesis, depending on the nature of their phenotypic changes. An in-depth characterization of their gene regulatory networks can help better understand how their dysfunction may impact disease progression.

methodsWe conducted a gene expression network preservation analysis in aortic smooth muscle cells isolated from 151 multiethnic heart transplant donors cultured under quiescent or proliferative conditions.

resultsWe identified 86 groups of coexpressed genes (modules) across the 2 conditions and focused on the 18 modules that are least preserved between the phenotypic conditions. Three of these modules were significantly enriched for genes belonging to proliferation, migration, cell adhesion, and cell differentiation pathways, characteristic of phenotypically modulated proliferative vascular smooth muscle cells. The majority of the modules, however, were enriched for metabolic pathways consisting of both nitrogen-related and glycolysis-related processes. Therefore, we explored correlations between nitrogen metabolism-related genes and coronary artery disease-associated genes and found significant correlations, suggesting the involvement of the nitrogen metabolism pathway in coronary artery disease pathogenesis. We also created gene regulatory networks enriched for genes in glycolysis and predicted key regulatory genes driving glycolysis dysregulation.

conclusionsOur work suggests that dysregulation of vascular smooth muscle cell metabolism participates in phenotypic transitioning, which may contribute to disease progression, and suggests that AMT (aminomethyltransferase) and MPI (mannose phosphate isomerase) may play an important role in regulating nitrogen and glycolysis-related metabolism in smooth muscle cells.

Indexed as

Coronary Artery DiseaseDisease ProgressionHumansMetabolic Networks and PathwaysMuscle, Smooth, VascularMyocytes, Smooth Muscleatherosclerosiscoronary artery diseaseglycolysisrisk factorsUnited States

Identifiers

PMID37387208
PMCPMC10434832
OpenAlexW4382631750

What OpenQuestion holds

Textmetadata
LicenceTDM
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.