ArticleGenome medicine2013
miR-638 regulates gene expression networks associated with emphysematous lung destruction.
Article in Genome medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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.
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.
Who cites it
43 citing papers in PubMed, 84 citations in OpenAlex.
- miR-495-3p promotes chronic obstructive pulmonary disease by activating ferroptosis in lung epithelial cells through regulation of the ETS1/GPX4 axis.Molecular biology reports · 2026Article
- Exercise and Epigenetic Regulation in COPD: Current Evidence and Potential Mechanistic Pathways.International journal of molecular sciences · 2025Review
- Computational identification of key genetic drivers in COPD: A first step towards uncovering candidate biomarkers in smokers.Biochemistry and biophysics reports · 2025Article
- Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The role of microRNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- 17β-Estradiol Abrogates TNF-α-Induced Human Brain Vascular Pericyte Migration by Downregulating miR-638 via ER-β.International journal of molecular sciences · 2024Article
- The Role of Exhaled Breath Condensate in Chronic Inflammatory and Neoplastic Diseases of the Respiratory Tract.International journal of molecular sciences · 2024Review
- Downregulation ofeLife · 2024Article
- Downregulation ofbioRxiv : the preprint server for biology · 2024Article
- TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase.Nature communications · 2023Article
- Review
- Integrative genetic and genomic networks identify microRNA associated with COPD and ILD.Scientific reports · 2023Article
- Air Pollution: Role of Extracellular Vesicles-Derived Non-Coding RNAs in Environmental Stress Response.Cells · 2023Review
- A Diagnostic Classifier Based on Circulating miRNA Pairs for COPD Using a Machine Learning Approach.Diagnostics (Basel, Switzerland) · 2023Article
- Plasma miR-150-5p as a Biomarker for Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
- Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?International journal of molecular sciences · 2022Review
- Article
- Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- The role of miRNAs in alveolar epithelial cells in emphysema.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease.JCI insight · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by varying degrees of emphysematous lung destruction and small airway disease, each with distinct effects on clinical outcomes. There is little known about how microRNAs contribute specifically to the emphysema phenotype. We examined how genome-wide microRNA expression is altered with regional emphysema severity and how these microRNAs regulate disease-associated gene expression networks.
methodsWe profiled microRNAs in different regions of the lung with varying degrees of emphysema from 6 smokers with COPD and 2 controls (8 regions × 8 lungs = 64 samples). Regional emphysema severity was quantified by mean linear intercept. Whole genome microRNA and gene expression data were integrated in the same samples to build co-expression networks. Candidate microRNAs were perturbed in human lung fibroblasts in order to validate these networks.
resultsThe expression levels of 63 microRNAs (P < 0.05) were altered with regional emphysema. A subset, including miR-638, miR-30c, and miR-181d, had expression levels that were associated with those of their predicted mRNA targets. Genes correlated with these microRNAs were enriched in pathways associated with emphysema pathophysiology (for example, oxidative stress and accelerated aging). Inhibition of miR-638 expression in lung fibroblasts led to modulation of these same emphysema-related pathways. Gene targets of miR-638 in these pathways were amongst those negatively correlated with miR-638 expression in emphysema.
conclusionsOur findings demonstrate that microRNAs are altered with regional emphysema severity and modulate disease-associated gene expression networks. Furthermore, miR-638 may regulate gene expression pathways related to the oxidative stress response and aging in emphysematous lung tissue and lung fibroblasts.
Identifiers
What OpenQuestion holds
Registered trials
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.