Evidence map›Paper›PMID 29330445›Full record

ArticleScientific reports2018

A novel approach for correction of crosstalk effects in pathway analysis and its application in osteoporosis research.

Yu Zhou, Yunlong Gao, Chao Xu, Hui Shen, Qing Tian, Hong-Wen Deng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing 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

54 citing papers in PubMed, 61 citations in OpenAlex.

  1. A microbiota-substrate-metabolite-target network suggests AKT1-associated links between gut microbiota-derived metabolites and osteoporosis.International microbiology : the official journal of the Spanish Society for Microbiology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Yu ZhouCenter of Genomics and Bioinformatics, Tulane University, New Orleans, LA, 70112, USA.
Yunlong GaoCenter of Genomics and Bioinformatics, Tulane University, New Orleans, LA, 70112, USA.
Chao XuCenter of Genomics and Bioinformatics, Tulane University, New Orleans, LA, 70112, USA.ORCID http://orcid.org/0000-0002-3821-6187
Hui ShenCenter of Genomics and Bioinformatics, Tulane University, New Orleans, LA, 70112, USA.
Qing TianCenter of Genomics and Bioinformatics, Tulane University, New Orleans, LA, 70112, USA.
Hong-Wen DengCenter of Genomics and Bioinformatics, Tulane University, New Orleans, LA, 70112, USA. hdeng2@tulane.edu.
Tulane University · US

Funding

Tulane COBRE in Cardiometabolic Diseases Clinical Research CoreP20GM109036 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI Ning Liu · 2016 to 2026
$25.3M
Trans-omics Integration of Multi-omics Studies for OsteoporosisU19AG055373 · NIA · TULANE UNIVERSITY OF LOUISIANA · PI Chuan Qiu · 2017 to 2026
$24.3M
Epigenomewide DNA Methylation Study for Osteoporosis RiskR01AR059781 · NIAMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, HONG-WEN · 2012 to 2016
$3.1M
Decoding Methylation Mediated Epigenomic Contributions to Male OsteoporosisR01AR069055 · NIAMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, HONG-WEN · 2017 to 2021
$2.9M
Integration of brain imaging with genomic and epigenomic dataR01MH104680 · NIMH · TULANE UNIVERSITY OF LOUISIANA · PI CALHOUN, VINCE D, DENG, HONG-WEN · 2014 to 2017
$2.1M
NIAMS NIH HHS R01 AR059781NIAMS NIH HHS R01 AR069055NIA NIH HHS U19 AG055373NIGMS NIH HHS P20 GM109036NIMH NIH HHS R01 MH104680
6 · The paper itself

Abstract

Osteoporosis is a prevalent bone metabolic disease and peripheral blood monocytes represent a major systemic cell type for bone metabolism. To identify the key dysfunctional pathways in osteoporosis, we performed pathway analyses on microarray data of monocytes from subjects with extremely high/low hip bone mineral density. We first performed a traditional pathway analysis for which different pathways were treated as independent. However, genes overlap among pathways will lead to "crosstalk" phenomenon, which may lead to false positive/negative results. Therefore, we applied correction techniques including a novel approach that considers the correlation among genes to adjust the crosstalk effects in the analysis. In traditional analysis, 10 pathways were found to be significantly associated with BMD variation. After correction for crosstalk effects, three of them remained significant. Moreover, the MAPK signaling pathway, which has been shown to be important for osteoclastogenesis, became significant only after the correction for crosstalk effects. We also identified a new module mainly consisting of genes present in mitochondria to be significant. In summary, we describe a novel method to correct the crosstalk effect in pathway analysis and found five key independent pathways involved in BMD regulation, which may provide a better understanding of biological functional networks in osteoporosis.

Indexed as

Gene Regulatory NetworksBone DensityFemaleGene Expression ProfilingHumansMAP Kinase Signaling SystemMiddle AgedMitochondriaOligonucleotide Array Sequence AnalysisOsteoporosis

Identifiers

PMID29330445
PMCPMC5766601
OpenAlexW2783629785

What OpenQuestion 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 OpenQuestion graph.