Evidence map›Paper›PMID 24789982›Full record

ReviewPhysiology (Bethesda, Md.)2014

Beyond the genome: epigenetic mechanisms in lung remodeling.

James S Hagood

Open access · greenAbstract readReview
In one paragraph

Review in Physiology (Bethesda, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Mucosal Immunity in Cystic Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Application of iPSC to Modelling of Respiratory Diseases.Advances in experimental medicine and biology · 2020
    Review
  15. Article
  16. Nicotine Modulates Growth Factors and MicroRNA to Promote Inflammatory and Fibrotic Processes.The Journal of pharmacology and experimental therapeutics · 2019
    Article
  17. Article
  18. Mechanisms for the Resolution of Organ Fibrosis.Physiology (Bethesda, Md.) · 2019
    Review
  19. Article
  20. The etiologic origins for chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2019
    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

1 author at 1 institution in 1 country.

James S HagoodDepartment of Pediatrics, Division of Respiratory Medicine, University of California-San Diego and Rady Children's Hospital of San Diego, San Diego, California.
University of California, San Diego · US

Funding

Regulation of Fibroblast Phenotype in Lung FibrosisR01HL082818 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAGOOD, JAMES S. · 2007 to 2017
$3.7M
Targeting the Apoptosis-Resistant Pulmonary MyofibroblastR01HL111169 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAGOOD, JAMES S. · 2012 to 2015
$1.7M
NHLBI NIH HHS HL-082818NHLBI NIH HHS HL-111169NHLBI NIH HHS R01 HL082818NHLBI NIH HHS R01 HL111169
6 · The paper itself

Abstract

The lung develops from a very simple outpouching of the foregut into a highly complex, finely structured organ with multiple specialized cell types that are required for its normal physiological function. During both the development of the lung and its remodeling in the context of disease or response to injury, gene expression must be activated and silenced in a coordinated manner to achieve the tremendous phenotypic heterogeneity of cell types required for homeostasis and pathogenesis. Epigenetic mechanisms, consisting of DNA base modifications such as methylation, alteration of histones resulting in chromatin modification, and the action of noncoding RNA, control the regulation of information "beyond the genome" required for both lung modeling and remodeling. Epigenetic regulation is subject to modification by environmental stimuli, such as oxidative stress, infection, and aging, and is thus critically important in chronic remodeling disorders such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), bronchopulmonary dysplasia (BPD), and pulmonary hypertension (PH). Technological advances have made it possible to evaluate genome-wide epigenetic changes (epigenomics) in diseases of lung remodeling, clarifying existing pathophysiological paradigms and uncovering novel mechanisms of disease. Many of these represent new therapeutic targets. Advances in epigenomic technology will accelerate our understanding of lung development and remodeling, and lead to novel treatments for chronic lung diseases.

Indexed as

AnimalsEpigenesis, GeneticGenomeHumansLung

Identifiers

PMID24789982
PMCPMC4046816
OpenAlexW2138585484

What OpenQuestion holds

Textmetadata
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.