Evidence map›Paper›PMID 36776884›Full record

ArticleFrontiers in immunology2023

Single-cell sequencing combined with machine learning reveals the mechanism of interaction between epilepsy and stress cardiomyopathy.

Xuanrui Ji, Quanwei Pei, Junpei Zhang, Pengqi Lin, Bin Li, Hongpeng Yin, Jingmei Sun, Dezhan Su, Xiufen Qu, Dechun Yin

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Review
  5. The role of inflammation in takotsubo syndrome: A new therapeutic target?Journal of cellular and molecular medicine · 2024
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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

10 authors at 2 institutions in 1 country.

Xuanrui JiDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Quanwei PeiDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Junpei ZhangDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Pengqi LinDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Bin LiDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Hongpeng YinDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jingmei SunDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Dezhan SuDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Xiufen QuDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Dechun YinDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Epilepsy is a disorder that can manifest as abnormalities in neurological or physical function. Stress cardiomyopathy is closely associated with neurological stimulation. However, the mechanisms underlying the interrelationship between epilepsy and stress cardiomyopathy are unclear. This paper aims to explore the genetic features and potential molecular mechanisms shared in epilepsy and stress cardiomyopathy. Methods: By analyzing the epilepsy dataset and stress cardiomyopathy dataset separately, the intersection of the two disease co-expressed differential genes is obtained, the co-expressed differential genes reveal the biological functions, the network is constructed, and the core modules are identified to reveal the interaction mechanism, the co-expressed genes with diagnostic validity are screened by machine learning algorithms, and the co-expressed genes are validated in parallel on the epilepsy single-cell data and the stress cardiomyopathy rat model. Results: Epilepsy causes stress cardiomyopathy, and its key pathways are Complement and coagulation cascades, HIF-1 signaling pathway, its key co-expressed genes include Conclusion: We believe epilepsy causing stress cardiomyopathy results from a multi-gene, multi-pathway combination. We identified the core co-expressed genes (

Indexed as

EpilepsyTakotsubo CardiomyopathyAnimalsGenes, MHC Class IIIntercellular Signaling Peptides and ProteinsMembrane ProteinsRatsSecreted Frizzled-Related ProteinsSignal TransductionIntercellular Signaling Peptides and ProteinsMembrane ProteinsSecreted Frizzled-Related ProteinsSfrp1 protein, ratepilepsyimmuno analysismachine learningmetabolic analysissingle-cell sequencingstress cardiomyopathystress cardiomyopathy rat model

Identifiers

PMID36776884
PMCPMC9911815
OpenAlexW4318200176

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Registered trials

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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.