Evidence map›Paper›PMID 31220921›Full record

ArticleCartilage2021

Integrative Analysis of Genome-Wide Association Studies and DNA Methylation Profile Identified Genetic Control Genes of DNA Methylation for Kashin-Beck Disease.

Ping Li, Cuiyan Wu, Xiong Guo, Yan Wen, Li Liu, Xiao Liang, Yanan Du, Lu Zhang, Mei Ma, Shiqiang Cheng and 3 more

Abstract read
In one paragraph

Article in Cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
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  4. 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

13 authors.

Ping LiKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.ORCID 0000-0002-0047-376X
Cuiyan WuKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Xiong GuoKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Yan WenKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Li LiuKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Xiao LiangKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Yanan DuKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Lu ZhangKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Mei MaKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Shiqiang ChengKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Bolun ChengKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Sen WangKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Feng ZhangKey Laboratory of Trace Elements and Endemic Disease of National Health Commission of the People's Republic of China, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveEpigenetic modifications of DNA are regarded as a crucial factor for understanding the molecular basis of complex phenotypes. This study aims to uncover insight into the epigenetic modifications for Kashin-Beck disease (KBD) by integrating genome-wide association studies (GWAS), methylation quantitative trait loci (meQTLs), and DNA methylation profiles data.

designThe knee articular cartilages of 5 KBD patients and 5 healthy controls were collected for DNA methylation profiling, using Illumina Infinium HumanMethylation450 BeadChip. Mass spectrograph validation of identified differently methylated genes was conducted using independent samples of 4 KBD patients and 3 healthy controls, together with a previous sample of 2743 Han Chinese individuals of GWAS study for KBD and a study of 697 normal subjects for meQTLs annotation datasets. KBD GWAS single nucleotide polymorphisms (SNPs) and normal meQTLs SNPs were integrated with DNA methylation profiles of KBD articular cartilage to identify genetic control (GC) genes of DNA methylation for KBD. Quantitative polymerase chain reaction (qPCR) was performed to validate the mRNA expression of several identified candidate genes.

resultsA total of 162 CpG sites, 253 SNPs, and 123 GC genes for KBD were identified. Enrichment analysis detected 642 marked GO terms and 19 KEGG pathways (

conclusionsThe results suggest that GC genes of DNA methylation may lead to the erosion of cartilage in KBD, which may help us in understanding the epigenetic alteration of KBD.

Indexed as

Cartilage, ArticularKashin-Beck DiseaseDNA MethylationGene Expression RegulationGenome-Wide Association StudyHumansDNA methylationgenetic control genesGWASKashin-Beck diseasemeQTLs

Identifiers

PMID31220921
PMCPMC8808895

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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.