Evidence map›Paper›PMID 42614776›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2026

Nuclear Factor Erythroid 2-Related Factor 2 in Chronic Obstructive Pulmonary Disease Progression: Regulation of Macrophage Polarization and Hyaluronic Acid Metabolism.

Ge Bai, Jiaqi Wang, Qianmei Wen, Yuning Huang, Haiqing Li, Yanhui Xu, Yiyi Liu, Erkang Yi, Fan Wu, Jieda Cui and 5 more

Abstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Ge Bai *State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Jiaqi Wang *Department of Pulmonary and Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, People's Republic of China.
Qianmei Wen *State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Yuning HuangGMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Haiqing LiState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.ORCID 0000-0003-4075-9356
Yanhui XuState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Yiyi LiuDepartment of Immunology, Guangzhou Institute of Paediatrics, Guangzhou Women and Children's Medical Centre, and State Key Laboratory of Respiratory Diseases, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Erkang YiGuangzhou National Laboratory, Guangzhou, Guangdong, People's Republic of China.
Fan WuState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.ORCID 0000-0003-0720-4674
Jieda CuiState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.ORCID 0000-0001-7970-0269
Xinyue MeiState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Yuxia ZhangDepartment of Immunology, Guangzhou Institute of Paediatrics, Guangzhou Women and Children's Medical Centre, and State Key Laboratory of Respiratory Diseases, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Yumin ZhouState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Ruiting SunState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Pixin RanState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Alveolar microenvironment-driven macrophage polarization critically influences chronic obstructive pulmonary disease (COPD) progression. Nuclear factor erythroid 2-related factor 2 (NRF2), a key transcription factor, regulates macrophage polarization, suppresses inflammation, and promotes cellular repair. However, its role in macrophage-mediated inflammation and metabolic regulation, particularly hyaluronic acid (HA)-related remodeling, remains incompletely defined. This study investigates a novel dimension of NRF2 in COPD pathogenesis through macrophage-specific modulation, aiming to uncover its previously unrecognized mechanism. Methods: Macrophage-specific Results: Conclusion: Macrophage-specific NRF2 protects against CS-induced COPD-like lung injury by restraining inflammatory activation and preserving macrophage polarization-associated balance. Proteomic and validation analyses further nominate HA metabolism-related remodeling, particularly the CD44/CD74-associated response, as a biologically plausible feature of NRF2-deficient disease progression. These findings define a macrophage NRF2-linked inflammatory-remodeling axis in COPD-like pathology while highlighting the need for functional studies to establish whether HA/CD44 signaling is a causal downstream mechanism.

Indexed as

Hyaluronic AcidLungMacrophage ActivationMacrophages, AlveolarNF-E2-Related Factor 2Pulmonary Disease, Chronic ObstructiveAirway RemodelingAnimalsCigarette SmokingCytokinesDisease Models, AnimalDisease ProgressionHyaluronan ReceptorsInflammation MediatorsMaleMice, Inbred C57BLCytokinesHyaluronan ReceptorsHyaluronic AcidInflammation MediatorsNfe2l2 protein, mouseNF-E2-Related Factor 2COPDhyaluronic acid metabolisminflammatory responsemacrophageNRF2

Identifiers

PMID42614776
PMCPMC13484630

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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.