Evidence map›Paper›PMID 31693390›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2020

Mitochondria: at the crossroads of regulating lung epithelial cell function in chronic obstructive pulmonary disease.

Mahyar Aghapour, Alexander H V Remels, Simon D Pouwels, Dunja Bruder, Pieter S Hiemstra, Suzanne M Cloonan, Irene H Heijink

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Molecular mechanisms underlying FCCP-induced mitophagy in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  3. Article
  4. Article
  5. Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Antioxidant Peptides fromMarine drugs · 2026
    Article
  12. Article
  13. Article
  14. Mitochondrial-derived microproteins in lung disease: insights and implications.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  15. β2-Microglobulin Induces Mitochondrial Dysfunction Accompanied by Bronchial Epithelial Cell Senescence.International journal of chronic obstructive pulmonary disease · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Mitochondria - the CEO of the cell.Journal of cell science · 2025
    Review
  20. Article

16 more citing papers are in PubMed but not listed here.

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

7 authors at 5 institutions in 3 countries.

Mahyar AghapourInfection Immunology Group, Institute of Medical Microbiology, Infection Control, and Prevention, Health Campus Immunology, Infectiology, and Inflammation, Otto-von-Guericke University, Magdeburg, Germany and Immune Regulation Group, Helmholtz Center for Infection Research, Braunschweig, Germany.ORCID 0000-0002-3548-3423
Alexander H V RemelsDepartment of Pharmacology and Toxicology, School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands.
Simon D PouwelsUniversity of Groningen, University Medical Center Groningen, Department of Pathology and Medical Biology, Groningen Research Institute for Asthma and COPD, Groningen, The Netherlands.ORCID 0000-0001-7345-8061
Dunja BruderInfection Immunology Group, Institute of Medical Microbiology, Infection Control, and Prevention, Health Campus Immunology, Infectiology, and Inflammation, Otto-von-Guericke University, Magdeburg, Germany and Immune Regulation Group, Helmholtz Center for Infection Research, Braunschweig, Germany.
Pieter S HiemstraDepartment of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-0238-5982
Suzanne M CloonanDivision of Pulmonary and Critical Care Medicine, Joan and Stanford I, Weill Department of Medicine, Weill Cornell Medical College, New York, New York.ORCID 0000-0001-5301-9926
Irene H HeijinkUniversity of Groningen, University Medical Center Groningen, Department of Pathology and Medical Biology, Groningen Research Institute for Asthma and COPD, Groningen, The Netherlands.
Helmholtz Centre for Infection Research · DEUniversity Medical Center Groningen · NLCornell University · USLeiden University Medical Center · NLMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disturbances in mitochondrial structure and function in lung epithelial cells have been implicated in the pathogenesis of various lung diseases, including chronic obstructive pulmonary disease (COPD). Such disturbances affect not only cellular energy metabolism but also alter a range of indispensable cellular homeostatic functions in which mitochondria are known to be involved. These range from cellular differentiation, cell death pathways, and cellular remodeling to physical barrier function and innate immunity, all of which are known to be impacted by exposure to cigarette smoke and have been linked to COPD pathogenesis. Next to their well-established role as the first physical frontline against external insults, lung epithelial cells are immunologically active. Malfunctioning epithelial cells with defective mitochondria are unable to maintain homeostasis and respond adequately to further stress or injury, which may ultimately shape the phenotype of lung diseases. In this review, we provide a comprehensive overview of the impact of cigarette smoke on the development of mitochondrial dysfunction in the lung epithelium and highlight the consequences for cell function, innate immune responses, epithelial remodeling, and epithelial barrier function in COPD. We also discuss the applicability and potential therapeutic value of recently proposed strategies for the restoration of mitochondrial function in the treatment of COPD.

Indexed as

AnimalsEpithelial CellsHumansLungMitochondriaNicotianaPulmonary Disease, Chronic ObstructiveRespiratory MucosaSmokingcigarette smokeCOPDlung epithelial cellsmitochondrial dysfunction

Identifiers

PMID31693390
PMCPMC6985875
OpenAlexW2983828143

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.