Evidence mapPaperPMID 39062733Full record

ArticleGenes2024

Transcriptomic Analysis of Arachidonic Acid Pathway Genes Provides Mechanistic Insight into Multi-Organ Inflammatory and Vascular Diseases.

Vaishnavi Aradhyula, Joshua D Breidenbach, Bella Z Khatib-Shahidi, Julia N Slogar, Sonia A Eyong, Dhilhani Faleel, Prabhatchandra Dube, Rajesh Gupta, Samer J Khouri, Steven T Haller and 1 more

Abstract read
In one paragraph

Article in Genes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
field-weighted citation impact
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

8 citing papers in PubMed.

  1. Multi-omics uncovers the critical role of ceramide-mediatedJournal of pharmaceutical analysis · 2026
    Article
  2. Article
  3. Review
  4. Observational
  5. Article
  6. Article
  7. Article
  8. 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

11 authors.

Vaishnavi AradhyulaDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Joshua D BreidenbachDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Bella Z Khatib-ShahidiDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Julia N SlogarDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.ORCID 0000-0003-2972-3678
Sonia A EyongDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Dhilhani FaleelDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Prabhatchandra DubeDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Rajesh GuptaDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Samer J KhouriDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Steven T HallerDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.ORCID 0000-0002-6919-6342
David J KennedyDepartment of Medicine, The University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.ORCID 0000-0001-5265-0142

Funding

The impact of episodic events on cHAB growth and secondary metabolite productionP01ES028939 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2024 to 2025
$1.6M
National Science Foundation OCE-1840715NHLBI NIH HHS R01 HL137004NIEHS NIH HHS P01 ES028939NIH HHS 2P01ES028939NIH HHS HL-137004
6 · The paper itself

Abstract

Arachidonic acid (AA) metabolites have been associated with several diseases across various organ systems, including the cardiovascular, pulmonary, and renal systems. Lipid mediators generated from AA oxidation have been studied to control macrophages, T-cells, cytokines, and fibroblasts, and regulate inflammatory mediators that induce vascular remodeling and dysfunction. AA is metabolized by cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP) to generate anti-inflammatory, pro-inflammatory, and pro-resolutory oxidized lipids. As comorbid states such as diabetes, hypertension, and obesity become more prevalent in cardiovascular disease, studying the expression of AA pathway genes and their association with these diseases can provide unique pathophysiological insights. In addition, the AA pathway of oxidized lipids exhibits diverse functions across different organ systems, where a lipid can be both anti-inflammatory and pro-inflammatory depending on the location of metabolic activity. Therefore, we aimed to characterize the gene expression of these lipid enzymes and receptors throughout multi-organ diseases via a transcriptomic meta-analysis using the Gene Expression Omnibus (GEO) Database. In our study, we found that distinct AA pathways were expressed in various comorbid conditions, especially those with prominent inflammatory risk factors. Comorbidities, such as hypertension, diabetes, and obesity appeared to contribute to elevated expression of pro-inflammatory lipid mediator genes. Our results demonstrate that expression of inflammatory AA pathway genes may potentiate and attenuate disease; therefore, we suggest further exploration of these pathways as therapeutic targets to improve outcomes.

Indexed as

Arachidonic AcidInflammationGene Expression ProfilingHumansTranscriptomeVascular DiseasesArachidonic Acidarachidonic acideicosanoidsinflammatory vascular remodelingtranscriptomicsvascular inflammation

Identifiers

PMID39062733
PMCPMC11275336

What Socratic 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 Socratic graph.