Evidence map›Paper›PMID 33240650›Full record

ArticlePeerJ2020

Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development.

Kai Zhang, Xianyu Qin, Xianwu Zhou, Jianrong Zhou, Pengju Wen, Shaoxian Chen, Min Wu, Yueheng Wu, Jian Zhuang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PeerJ, 2020. 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
0.8field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. FromCells · 2022
    Review
  5. Article
  6. Article
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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

9 authors at 3 institutions in 1 country.

Kai ZhangDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Xianyu QinDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Xianwu ZhouDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Jianrong ZhouDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Pengju WenDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Shaoxian ChenDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Min WuDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Yueheng WuDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Jian ZhuangDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangdong Cardiovascular Institute, Guangzhou, Guangdong, China.
Guangdong Academy of Medical Sciences · CNGuangdong Provincial People's Hospital · CNSouth China University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFoam cells (FCs) play crucial roles in the process of all stages of atherosclerosis. Smooth muscle cells (SMCs) and macrophages are the major sources of FCs. This study aimed to identify the common molecular mechanism in these two types of FCs.

methodsGSE28829, GSE43292, GSE68021, and GSE54666 were included to identify the differentially expressed genes (DEGs) associated with FCs derived from SMCs and macrophages. Gene Ontology biological process (GO-BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed by using the DAVID database. The co-regulated genes associated with the two origins of FCs were validated (GSE9874), and their expression in vulnerable atherosclerosis plaques (GSE120521 and GSE41571) was assessed.

resultsA total of 432 genes associated with FCs derived from SMCs (SMC-FCs) and 81 genes associated with FCs derived from macrophages (M-FCs) were identified, and they were mainly involved in lipid metabolism, inflammation, cell cycle/apoptosis. Furthermore, three co-regulated genes associated with FCs were identified:

conclusionsDEGs related to FCs derived from SMCs and macrophages have contributed to the understanding of the molecular mechanism underlying the formation of FCs and atherosclerosis.

Indexed as

AtherosclerosisDifferentially expressed genesFoam cellsMacrophagesSmooth muscle cells

Identifiers

PMID33240650
PMCPMC7678445
OpenAlexW3100819272

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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.