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Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...
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Predisposition for disrepair in the aged lung.
Viranuj Sueblinvong1, David C Neujahr, S Todd Mills
1Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30032, USA. vsuebli@emory.edu
The American Journal of the Medical Sciences
|December 17, 2011
Summary
Aged lungs exhibit a profibrotic phenotype, increasing susceptibility to lung fibrosis. This involves enhanced fibronectin and matrix metalloproteinase expression, alongside increased TGF-β1 signaling, contributing to age-related lung disease.
Area of Science:
- Pulmonary Medicine
- Aging Research
- Fibrosis Pathogenesis
Background:
- Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with poor prognosis.
- Aging is a significant risk factor for IPF, but underlying mechanisms remain unclear.
- Aged lungs may possess an inherent profibrotic state predisposing them to injury.
Purpose of the Study:
- To investigate the profibrotic phenotype of aged lungs.
- To identify age-associated changes in lung tissue and fibroblasts.
- To explore potential epigenetic contributions to age-related lung fibrosis.
Main Methods:
- Comparison of bleomycin-induced lung injury in young versus old mice.
- Analysis of extracellular matrix, TGF-β1, and fibroblast markers in aged and young lungs.
- In vitro study of aged lung fibroblasts with DNA methyltransferase inhibitors.
Main Results:
- Old mice exhibited exacerbated lung fibrosis post-injury.
- Aged lungs showed increased fibronectin (Fn-EDA) and matrix metalloproteinase (MMP) expression.
- Elevated TGF-β1 signaling and reduced Thy-1 expression were observed in aged lung fibroblasts.
Conclusions:
- Aged lungs possess a profibrotic phenotype, characterized by specific molecular markers.
- Enhanced fibronectin, MMP, and TGF-β1 signaling contribute to age-related lung fibrosis.
- Thy-1-negative fibroblasts in aged lungs are implicated in fibrosis pathogenesis.