Evidence map›Paper›PMID 39125750›Full record

ArticleInternational journal of molecular sciences2024

Role of ATG4 Autophagy-Related Protein Family in the Lower Airways of Patients with Stable COPD.

Francesco Nucera, Antonino Di Stefano, Fabio Luigi Massimo Ricciardolo, Isabella Gnemmi, Cristina Pizzimenti, Francesco Monaco, Giovanni Tuccari, Gaetano Caramori, Antonio Ieni

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Francesco NuceraDepartment of Biomedical, Dental, Morphological and Functional Imaging Sciences, Section of Pneumology, University of Messina, 98125 Messina, Italy.ORCID 0000-0001-8454-5363
Antonino Di StefanoIstituti Clinici Scientifici Maugeri, IRCCS, Respiratory Rehabilitation Unit of Gattico-Veruno, Section of Pneumology, Laboratory of Cytoimmunopathology in Cardio Respiratory System, 28013 Gattico-Veruno, Italy.ORCID 0000-0003-3479-0875
Fabio Luigi Massimo RicciardoloDepartment of Clinical and Biological Sciences, Severe Asthma, Rare Lung Disease and Respiratory Pathophysiology Unit, San Luigi Gonzaga University Hospital, University of Turin, 10043 Orbassano, Italy.ORCID 0000-0003-1826-5018
Isabella GnemmiIstituti Clinici Scientifici Maugeri, IRCCS, Respiratory Rehabilitation Unit of Gattico-Veruno, Section of Pneumology, Laboratory of Cytoimmunopathology in Cardio Respiratory System, 28013 Gattico-Veruno, Italy.ORCID 0000-0003-0045-6369
Cristina PizzimentiDepartment of Human Pathology in Adult and Developmental Age 'Gaetano Barresi', Section of Pathology, University of Messina, 98125 Messina, Italy.ORCID 0000-0002-4387-7174
Francesco MonacoDepartment of Biomedical, Dental, Morphological and Functional Imaging Sciences, Section of Toracic Surgery, University of Messina, 98125 Messina, Italy.ORCID 0000-0002-5617-7943
Giovanni TuccariDepartment of Human Pathology in Adult and Developmental Age 'Gaetano Barresi', Section of Pathology, University of Messina, 98125 Messina, Italy.ORCID 0000-0002-1561-4246
Gaetano CaramoriDepartment of Medicine and Surgery, Sections of Pneumology, University of Parma, 43126 Parma, Italy.ORCID 0000-0002-9807-327X
Antonio IeniDepartment of Human Pathology in Adult and Developmental Age 'Gaetano Barresi', Section of Pathology, University of Messina, 98125 Messina, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a complex physiological pathway mediating homeostasis and survival of cells degrading damaged organelles and regulating their recycling. Physiologic autophagy can maintain normal lung function, decrease lung cellular senescence, and inhibit myofibroblast differentiation. It is well known that autophagy is activated in several chronic inflammatory diseases; however, its role in the pathogenesis of chronic obstructive pulmonary disease (COPD) and the expression of autophagy-related genes (ATGs) in lower airways of COPD patients is still controversial. The expression and localization of all ATG proteins that represented key components of the autophagic machinery modulating elongation, closure, and maturation of autophagosome membranes were retrospectively measured in peripheral lungs of patients with stable COPD (

Indexed as

AutophagyAutophagy-Related ProteinsPulmonary Disease, Chronic ObstructiveAgedCysteine EndopeptidasesFemaleHumansLungMaleMiddle AgedSmokingATG4A protein, humanATG4B protein, humanAutophagy-Related ProteinsCysteine EndopeptidasesATG4autophagychronic obstructive pulmonary diseaselung diseasetreatment

Identifiers

PMID39125750
PMCPMC11311497

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.