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Deciphering Pathogenesis of Silica Nanoparticle-Induced Airway Remodeling and Fibrosis: Insights from a Human Patient Cohort and a Murine Model Full article

Journal Nanomaterials
ISSN: 2079-4991
Output data Year: 2026, Volume: 16, Article number : 866, Pages count : 27 DOI: 10.3390/nano16140866
Tags occupational COPD; nanoparticles; silicon dioxide; clinical cohort; in vivo model
Authors Sen’kova A.V. 1 , Savin I.A. 1 , Kotova O.S. 2 , Shpagin I.S. 2 , Dmitrienko E.V. 1 , Popova V.K. 1 , Khasanov B.R. 1 , Tsygankova A.R. 3 , Markov O.V. 1 , Awad M.S. 1 , Saprykin A.I. 3 , Shpagina L.A. 2 , Vlasov V.V. 1 , Zenkova M.A. 1
Affiliations
1 Knorre Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences
2 Department of Hospital Therapy and Medical Rehabilitation, Novosibirsk State Medical University
3 Nikolaev Institute of Inorganic Chemistry, Siberian Branch of the Russian Academy of Sciences

Funding (1)

1

Abstract: Occupational chronic obstructive pulmonary disease (O-COPD) represents a lung disorder attributable to occupational exposures that are characterized by early development of airway remodeling and pulmonary fibrosis. O-COPD is poorly recapitulated by existing preclinical models. This study aimed to perform comparative characterization of an OCOPD patient cohort exposed to industrial aerosols and to develop a relevant murine model that accurately mirrors the human pathology. In the patient cohort, it was shown that the O-COPD phenotype is associated with the chemical composition of industrial aerosols and mediated by a specific inflammatory pattern with predominant obstructive changes and increased bronchial reactivity upon exposure to metal particles, as well as irreversible fibrotic changes in the lungs upon exposure to silicon dioxide. In the murine model, silica nanoparticles (SiNPs) or magnetic nanoparticles (MNPs) were utilized. Repeated intranasal SiNP administrations have been shown to reflect one of the main features of O-COPD—progressive airway remodeling and fibrosis, observed even after elimination of SiNPs. Administration of MNPs in the same regimen did not result in fibrotic changes in the lungs, partially recapitulating the human pathology resulting from exposure to the complex composition of industrial aerosols as well as the specific properties of chemically synthesized nanoparticles. Thus, the integrative data from the human cohort and animal model provides a reflective platform to advance the investigation of O-COPD mechanisms and development of interventions for fibrotic lung pathology. Keywords: occupational COPD; nanoparticles; silicon dioxide; clinical cohort; in vivo model.
Cite: Sen’kova A.V. , Savin I.A. , Kotova O.S. , Shpagin I.S. , Dmitrienko E.V. , Popova V.K. , Khasanov B.R. , Tsygankova A.R. , Markov O.V. , Awad M.S. , Saprykin A.I. , Shpagina L.A. , Vlasov V.V. , Zenkova M.A.
Deciphering Pathogenesis of Silica Nanoparticle-Induced Airway Remodeling and Fibrosis: Insights from a Human Patient Cohort and a Murine Model
Nanomaterials. 2026. V.16. 866 :1-27. DOI: 10.3390/nano16140866 WOS Scopus OpenAlex
Dates:
Submitted: Jun 17, 2026
Published print: Jul 15, 2026
Identifiers:
≡ Web of science: WOS:001833052100001
≡ Scopus: 2-s2.0-105045903003
≡ OpenAlex: W7168427708
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