Evidence map›Paper›PMID 36435742›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

Modular networks and genomic variation during progression from stable angina pectoris through ischemic cardiomyopathy to chronic heart failure.

Lin Chen, Ya-Nan Yu, Jun Liu, Yin-Ying Chen, Bo Wang, Yi-Fei Qi, Shuang Guan, Xi Liu, Bing Li, Ying-Ying Zhang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

12 authors at 3 institutions in 1 country.

Lin Chen *Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China.
Ya-Nan Yu *Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China.
Jun LiuInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China.
Yin-Ying ChenGuang'anmen Hospital, China Academy of Chinese Medical Sciences, No. 5 Beixian Ge, Xicheng District, Beijing, 100053, China.
Bo WangInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China.
Yi-Fei QiXi Yuan Hospital, China Academy of Chinese Medical Sciences, No. 1, Xiyuan Playground, Haidian District, Beijing, 100091, China.
Shuang GuanInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China.
Xi LiuInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China.
Bing LiInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Dongzhimen, Beijing, 100700, China.
Ying-Ying ZhangGeriatric Department, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Dongzhimen, Beijing, 100007, China.
Yuanhui HuGuang'anmen Hospital, China Academy of Chinese Medical Sciences, No. 5 Beixian Ge, Xicheng District, Beijing, 100053, China. huiyuhui55@sohu.com.
Zhong WangInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China. zhonw@vip.sina.com.ORCID 0000-0003-0975-9251
Chinese Academy of Medical Sciences & Peking Union Medical College · CNDongzhimen Hospital Affiliated to Beijing University of Chinese Medicine · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnalyzing disease-disease relationships plays an important role for understanding etiology, disease classification, and drug repositioning. However, as cardiovascular diseases with causative links, the molecular relationship among stable angina pectoris (SAP), ischemic cardiomyopathy (ICM) and chronic heart failure (CHF) is not clear.

methodsIn this study, by integrating the multi-database data, we constructed paired disease progression modules (PDPMs) to identified relationship among SAP, ICM and CHF based on module reconstruction pairs (MRPs) of K-value calculation (a Euclidean distance optimization by integrating module topology parameters and their weights) methods. Finally, enrichment analysis, literature validation and structural variation (SV) were performed to verify the relationship between the three diseases in PDPMs.

resultsTotal 16 PDPMs were found with K > 0.3777 among SAP, ICM and CHF, in which 6 pairs in SAP-ICM, 5 pairs for both ICM-CHF and SAP-CHF. SAP-ICM was the most closely related by having the smallest average K-value (K = 0.3899) while the maximum is SAP-CHF (K = 0.4006). According to the function of the validation gene, inflammatory response were through each stage of SAP-ICM-CHF, while SAP-ICM was uniquely involved in fibrosis, and genes were related in affecting the upstream of PI3K-Akt signaling pathway. 4 of the 11 genes (FLT1, KDR, ANGPT2 and PGF) in SAP-ICM-CHF related to angiogenesis in HIF-1 signaling pathway. Furthermore, we identified 62.96% SVs were protein deletion in SAP-ICM-CHF, and 53.85% SVs were defined as protein replication in SAP-ICM, while ICM-CHF genes were mainly affected by protein deletion.

conclusionThe PDPMs analysis approach combined with genomic structural variation provides a new avenue for determining target associations contributing to disease progression and reveals that inflammation and angiogenesis may be important links among SAP, ICM and CHF progression.

Indexed as

Angina, StableCardiomyopathiesHeart FailureMyocardial IschemiaChronic DiseaseDisease ProgressionGenomicsHumansPhosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesGenomic variationModular networksModule reconstruction pairs

Identifiers

PMID36435742
PMCPMC9701405
OpenAlexW4310272643

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.