Evidence map›Paper›PMID 35008971›Full record

ReviewInternational journal of molecular sciences2022

Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?

Edibe Avci, Pouya Sarvari, Rajkumar Savai, Werner Seeger, Soni S Pullamsetti

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Advances in sirtuin research in lung diseases (Review).International journal of molecular medicine · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Beyond genes: a clinician's guide to epigenetics.Breathe (Sheffield, England) · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024
    Review
  14. Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  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

5 authors.

Edibe AvciDepartment of Lung Development and Remodeling, Max-Planck Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany.ORCID 0000-0002-8446-4712
Pouya SarvariDepartment of Lung Development and Remodeling, Max-Planck Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany.
Rajkumar SavaiDepartment of Lung Development and Remodeling, Max-Planck Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany.ORCID 0000-0003-1538-2091
Werner SeegerDepartment of Lung Development and Remodeling, Max-Planck Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany.
Soni S PullamsettiDepartment of Lung Development and Remodeling, Max-Planck Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany.ORCID 0000-0003-0440-8831

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic responses due to environmental changes alter chromatin structure, which in turn modifies the phenotype, gene expression profile, and activity of each cell type that has a role in the pathophysiology of a disease. Pulmonary diseases are one of the major causes of death in the world, including lung cancer, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH), lung tuberculosis, pulmonary embolism, and asthma. Several lines of evidence indicate that epigenetic modifications may be one of the main factors to explain the increasing incidence and prevalence of lung diseases including IPF and COPD. Interestingly, isolated fibroblasts and smooth muscle cells from patients with pulmonary diseases such as IPF and PH that were cultured ex vivo maintained the disease phenotype. The cells often show a hyper-proliferative, apoptosis-resistant phenotype with increased expression of extracellular matrix (ECM) and activated focal adhesions suggesting the presence of an epigenetically imprinted phenotype. Moreover, many abnormalities observed in molecular processes in IPF patients are shown to be epigenetically regulated, such as innate immunity, cellular senescence, and apoptotic cell death. DNA methylation, histone modification, and microRNA regulation constitute the most common epigenetic modification mechanisms.

Indexed as

Disease SusceptibilityEpigenesis, GeneticGene Expression RegulationAnimalsBiomarkersCombined Modality TherapyDiagnosis, DifferentialDisease ManagementDNA MethylationHistonesHumansIdiopathic Pulmonary FibrosisLung Diseases, InterstitialPulmonary Disease, Chronic ObstructiveTreatment OutcomeBiomarkersHistonesCOPDDNA methylationepigenetic editinggene transferhistone modificationsIPFmicroRNA

Identifiers

PMID35008971
PMCPMC8745712

What OpenQuestion holds

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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.