Evidence map›Paper›PMID 40860610›Full record

ReviewInternational journal of chronic obstructive pulmonary disease2025

Pathogenic Cell in COPD: Mechanisms of Airway Remodeling, Immune Dysregulation, and Therapeutic Implications.

Kailin Zhou, Qianmei Wen, Yujie Zuo, Ge Bai, Ruiting Sun

Abstract readReview
In one paragraph

Review in International journal of chronic obstructive pulmonary disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
–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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  6. Review
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  11. Observational
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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.

Kailin ZhouState Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, People's Republic of China.ORCID 0009-0001-5881-706X
Qianmei WenState Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, People's Republic of China.
Yujie ZuoState Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, People's Republic of China.
Ge BaiState Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, People's Republic of China.
Ruiting SunState Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathological alterations in COPD cells represent adaptive responses to COPD lesions, focusing on three primary pathological changes: abnormal repair and tissue remodeling, protease-antiprotease imbalance, and inflammatory amplification alongside immune disorder. These alterations ultimately result in a detrimental cycle of lung parenchymal destruction and airway structural remodeling. COPD manifests with diverse pathological phenotypes, pronounced heterogeneity, and a convoluted evolution process. However the role of pathological changes and mechanisms in pathological cells, as well as cellular senescence, metabolic reprogramming, and intercellular interaction networks in COPD, remains unclear. This review comprehensively encapsulates the most recent research advancements regarding the principal pathological cells in COPD, encompassing airway epithelial cells, fibroblasts, endothelial cells, and immune inflammatory cells. Elucidated the pathological alterations of these cells in relation to COPD, their influence on disease progression, and their clinical implications. Furthermore, Exosome-mediated miRNA transfer exacerbates inflammation and fibrosis, suggesting novel therapeutic targets. In summary, our work aims to provide a basic reference for research into the pathogenic mechanisms of this disease.

Indexed as

Airway RemodelingEpithelial CellsLungPulmonary Disease, Chronic ObstructiveAnimalsEndothelial CellsFibroblastsHumansInflammation MediatorsMicroRNAsSignal TransductionInflammation MediatorsMicroRNAsairway epithelial cellscellular senescencechronic obstructive pulmonary diseaseendothelial cellsextracellular vesiclesfibroblastsimmune inflammatory cellsmiRNANETosis

Identifiers

PMID40860610
PMCPMC12377387

What Socratic 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 Socratic graph.