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Updated: Apr 6, 2026
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Exposure to fine airborne particulate matters induces hepatic fibrosis in murine models
Ze Zheng1, Xuebao Zhang1, Jiemei Wang1
1Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Background & Aims:
Hepatic fibrosis, featured by the accumulation of excessive extracellular matrix in liver tissue, is associated with metabolic disease and cancer. Inhalation exposure to airborne particulate matter in fine ranges (PM2.5) correlates with pulmonary dysfunction, cardiovascular disease, and metabolic syndrome. In this study, we investigated the effect and mechanism of PM2.5 exposure on hepatic fibrogenesis.
Methods:
Both inhalation exposure of mice and in vitro exposure of specialized cells to PM2.5 were performed to elucidate the effect of PM2.5 exposure on hepatic fibrosis. Histological examinations, gene expression analyses, and genetic animal models were utilized to determine the effect and mechanism by which PM2.5 exposure promotes hepatic fibrosis.
Results:
Inhalation exposure to concentrated ambient PM2.5 induces hepatic fibrosis in mice under the normal chow or high-fat diet. Mice after PM2.5 exposure displayed increased expression of collagens in liver tissues. Exposure to PM2.5 led to activation of the transforming growth factor β-SMAD3 signaling, suppression of peroxisome proliferator-activated receptor γ, and expression of collagens in hepatic stellate cells. NADPH oxidase plays a critical role in PM2.5-induced liver fibrogenesis.
Conclusions:
Exposure to PM2.5 exerts discernible effects on promoting hepatic fibrogenesis. NADPH oxidase mediates the effects of PM2.5 exposure on promoting hepatic fibrosis.
Insights
Exposure to fine particulate matter (PM2.5) promotes liver fibrosis by activating specific cellular pathways. NADPH oxidase is identified as a key mediator in this process, highlighting a novel mechanism for PM2.5-induced liver damage.
Area of Science:
- Environmental Health
- Toxicology
- Hepatology
Background:
- Hepatic fibrosis, characterized by excessive extracellular matrix deposition, is linked to metabolic diseases and cancer.
- Inhalation of fine particulate matter (PM2.5) is associated with various health issues, including cardiovascular and metabolic diseases.
Purpose of the Study:
- To investigate the impact of PM2.5 exposure on hepatic fibrogenesis.
- To elucidate the underlying mechanisms of PM2.5-induced liver fibrosis.
Main Methods:
- In vivo mouse models and in vitro cell culture exposed to PM2.5.
- Histological examination, gene expression analysis, and genetic models to assess fibrosis.
- Analysis of transforming growth factor β-SMAD3 signaling and peroxisome proliferator-activated receptor γ.
Main Results:
- PM2.5 inhalation induced hepatic fibrosis in mice on normal and high-fat diets.
- Increased collagen expression and activation of TGF-β-SMAD3 signaling were observed.
- PM2.5 exposure suppressed PPARγ and activated NADPH oxidase in hepatic stellate cells.
Conclusions:
- PM2.5 exposure significantly promotes hepatic fibrogenesis.
- NADPH oxidase plays a crucial role in mediating PM2.5-induced liver fibrosis.
