Evidence map›Paper›PMID 29522352›Full record

ArticleAmerican journal of respiratory cell and molecular biology2018

Early Endotyping: A Chance for Intervention in Chronic Obstructive Pulmonary Disease.

Hans Petersen, Rodrigo Vazquez Guillamet, Paula Meek, Akshay Sood, Yohannes Tesfaigzi

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–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

13 citing papers in PubMed.

  1. Endotyping COPD: hypoxia-inducible factor-2 as a molecular "switch" between the vascular and airway phenotypes?European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Functional Gene Variants in Chronic Obstructive Pulmonary Disease: The Search Continues.American journal of respiratory cell and molecular biology · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. B Cell-Adaptive Immune Profile in Emphysema-Predominant Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2019
    Article
  12. COPD: To Be or Not to Be, That is the Question.The American journal of medicine · 2019
    Review
  13. 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

5 authors.

Hans Petersen1 COPD Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico.
Rodrigo Vazquez Guillamet2 Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico; and.
Paula Meek3 Adult and Gerontological Health Division, University of Colorado College of Nursing, Colorado.
Akshay Sood2 Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico; and.
Yohannes Tesfaigzi1 COPD Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico.ORCID 0000-0002-3997-5839

Funding

Resolution of Epithelial Cell Hyperplasia in AsthmaR01HL068111 · NHLBI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI TESFAIGZI, YOHANNES · 2003 to 2021
$10.9M
Resolution of Epithelial Cell HyperplasiaR01ES015482 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI TESFAIGZI, YOHANNES · 2009 to 2013
$2.6M
Regulation of Mucous Cell Metaplasia in AsthmaR56HL068111 · NHLBI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI TESFAIGZI, YOHANNES · 2007 to 2007
$500k
NHLBI NIH HHS R01 HL068111NHLBI NIH HHS R56 HL068111NIEHS NIH HHS R01 ES015482
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a syndrome that comprises several lung pathologies, but subphenotyping the various disease subtypes has been difficult. One reason may be that current efforts focused on studying COPD once it has occurred do not allow tracing back to the different origins of disease. This perspective proposes that emphysema originates when susceptible airway, endothelial, and/or hematopoietic cells are exposed to environmental toxins such as cigarette smoke, biomass fuel, or traffic emissions. These susceptible cell types may initiate distinct pathobiological mechanisms ("COPD endotypes") that ultimately manifest the emphysematous destruction of the lung. On the basis of evidence from the "airway" endotype, we suggest that grading these endotypes by severity may allow better diagnosis of disease at early stages when intervention can be designed on the basis of the mechanisms involved. Therefore, genomic, proteomic, and metabolomic studies on at-risk patients will be important in the identification of biomarkers that help designate each endotype. Together with understanding of the involved molecular pathways that lead to disease manifestation, these efforts may lead to development of intervention strategies.

Indexed as

Airway RemodelingAnimalsBiomarkersEndophenotypesGenome-Wide Association StudyHumansPulmonary Disease, Chronic ObstructiveBiomarkersairwayendotheliahematopoieticlung cell typessusceptibility

Identifiers

PMID29522352
PMCPMC6039877

What OpenQuestion holds

Textmetadata
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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.