Evidence map›Paper›PMID 31016901›Full record

ReviewYonsei medical journal2019

COPD as a Disease of Immunosenescence.

Won Kyung Cho, Chun Geun Lee, Lark Kyun Kim

Open access · goldAbstract readReview
In one paragraph

Review in Yonsei medical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 3 pooled it
5.9field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 3 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Frailty and COPD: a bidirectional relationship in the context of systemic and accelerated ageing.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  6. Review
  7. Review
  8. Immunosenescence: signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025
    Review
  9. Article
  10. Role of Regulatory T Cells in Pulmonary Ageing and COPD Development.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 3 institutions in 2 countries.

Won Kyung ChoDepartment of Pulmonary and Critical Care Medicine, International Healthcare Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. wonkyungcho@amc.seoul.kr.ORCID https://orcid.org/0000-0003-1540-545X
Chun Geun LeeDepartment of Molecular Microbiology and Immunology, Division of Biology and Medical Sciences, Brown University, Providence, RI, USA.ORCID https://orcid.org/0000-0002-9514-3658
Lark Kyun KimSeverance Biomedical Science Institute and BK21 PLUS Project for Medical Sciences, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. lkkim@yuhs.ac.ORCID https://orcid.org/0000-0001-5983-4470
Asan Medical Center · KRBrown University · USSeverance Hospital · KR

Funding

Genetic Factors Controlling Effector Function of TGF-beta in COPD and FibrosisR01HL084225 · NHLBI · YALE UNIVERSITY · PI LEE, CHUN GEUN · 2007 to 2011
$2.4M
Chitinase1 as a Biomarker and Therapeutic Target in Scleroderma Lung DiseaseR01HL115813 · NHLBI · BROWN UNIVERSITY · PI LEE, CHUN GEUN · 2014 to 2017
$1.5M
National Research Foundation of Korea NRF-2016R1D1A1B01015292NHLBI NIH HHS R01 HL084225NHLBI NIH HHS R01 HL115813
6 · The paper itself

Abstract

Although chronic obstructive pulmonary disease (COPD) is regarded as a chronic inflammatory lung disease, the disease mechanism is still not known. Intriguingly, aging lungs are quite similar to COPD-affected lungs in many ways, and COPD has been viewed as a disease of accelerated premature aging of the lungs. In this paper, based on a literature review, we would like to propose immunosenescence, age-associated decline in immunity, as a critical mechanism for the development of COPD. Immunosenescence can cause a low-grade, systemic inflammation described as inflammaging. This inflammaging may be directly involved in the COPD pathogenesis. The potential contributors to the development of inflammaging in the lungs possibly leading to COPD are discussed in the review paper. A notable fact about COPD is that only 15% to 20% of smokers develop clinically significant COPD. Given that there is a substantial inter-individual variation in inflammaging susceptibility, which is genetically determined and significantly affected by the history of the individual's exposure to pathogens, immunosenescence and inflammaging may also provide the answer for this unexpectedly low susceptibility of smokers to clinically significant COPD.

Indexed as

ImmunosenescenceAgingHumansInflammationLungPulmonary Disease, Chronic ObstructiveagingCOPDimmunosenescenceinflammaginginflammation

Identifiers

PMID31016901
PMCPMC6479124
OpenAlexW2941105289

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.