Evidence map›Paper›PMID 30221703›Full record

ArticleMolecular medicine reports2018

Molecular pathogenesis involved in human idiopathic pulmonary fibrosis based on an integrated microRNA‑mRNA interaction network.

Lijing Wang, Wei Huang, Lemeng Zhang, Qiong Chen, Hongjun Zhao

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. 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

5 authors at 4 institutions in 2 countries.

Lijing WangDepartment of Gerontology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Wei HuangDivision of Cellular Therapy, Duke University, Durham, NC 27710, USA.
Lemeng ZhangDepartment of Thoracic Oncology, Hunan Cancer Hospital, Changsha, Hunan 410008, P.R. China.
Qiong ChenDepartment of Gerontology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Hongjun ZhaoDepartment of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Xiangya Hospital Central South University · CNCentral South University · CNDuke University · USHunan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is considered to be an ailment of the lungs that cannot be cured, wherein the lung tissues are characterized by increased thickness and stiffness, and/or scars. Despite the fact that extensive success has been achieved regarding the molecular diagnostics and pathobiology, the basic pathogenesis associated with IPF has not yet been fully elucidated and requires further clarification. In the current research, the changes in microRNA (miRNA) and mRNA expression in IPF were investigated through an integrative network technique. The authentic miRNA and mRNA expression profiling datasets were downloaded from Gene Expression Omnibus, followed by identification of differentially expressed miRNAs and mRNAs with use of the Significance Analysis of Microarrays algorithm. Expansion of the molecular targets associated with miRNAs was performed with the use of CyTargetLinker in Cytoscape, which was succeeded by validation with the use of mRNA array expression profiling. The incorporated miRNA‑mRNA network covered 27 genes, in addition to 22 miRNAs that were associated with IPF development. As revealed by the functional enrichment analysis, the cytokine‑cytokine receptor interaction and glycine, serine and threonine metabolism signalling pathways were extensively associated with IPF development. Overall, the present incorporated network illustrated the key link between miRNA and genes in IPF; in particular, it was elucidated that miR‑409‑5p and has‑miR‑376c, together with their target genes (C‑C motif chemokine ligand 20 and oncostatin M), are likely candidates involved in the promotion of IPF initiation and progression.

Indexed as

Disease ProgressionFemaleGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansIdiopathic Pulmonary FibrosisLungMaleMicroRNAsNeoplasm ProteinsOligonucleotide Array Sequence AnalysisOncostatin MRNA, MessengerMicroRNAsMIRN409 microRNA, humanNeoplasm ProteinsOncostatin MRNA, Messenger

Identifiers

PMID30221703
PMCPMC6172385
OpenAlexW2891911746

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.