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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Oxidative stress and pulmonary fibrosis
Paul Cheresh1, Seok-Jo Kim, Sandhya Tulasiram
1Department of Medicine, Northwestern University Feinberg School of Medicine and Jesse Brown VA Medical Center, USA.
Biochimica Et Biophysica Acta
|December 11, 2012
Summary
Reactive oxygen species (ROS) drive pulmonary fibrosis through various cellular pathways. Understanding ROS origins and their impact on DNA damage and cell death offers new therapeutic targets for lung fibrosis.
Area of Science:
- Biomedical Science
- Molecular Biology
- Pathology
Background:
- Oxidative stress is a key factor in organ fibrosis, particularly pulmonary fibrosis.
- The precise role of reactive oxygen species (ROS) in fibrosis development and effective therapeutic targeting remains unclear.
Purpose of the Study:
- To review the origins and molecular mechanisms of oxidative stress in pulmonary fibrosis.
- To examine the role of ROS in lung epithelial cell apoptosis and endoplasmic reticulum stress.
- To explore the interplay between ROS, DNA damage, and repair pathways in fibrosis.
Main Methods:
- Review of existing literature on oxidative stress and pulmonary fibrosis.
- Analysis of molecular pathways involving ROS, cell death, and DNA repair.
- Discussion of the link between ROS and transforming growth factor-beta 1 (TGF-β1) in fibrosis.
Main Results:
- Key sources of oxidative stress in pulmonary fibrosis include environmental toxins, cellular oxidases, and depleted antioxidant defenses.
- Mitochondrial and p53-regulated pathways contribute to alveolar epithelial cell apoptosis.
- Mitochondrial DNA damage, particularly involving 8-oxoguanine DNA glycosylase (Ogg1), plays a significant role, interacting with ROS, p53, and ACO2.
Conclusions:
- Novel insights into ROS-mediated lung epithelial cell death can inform the development of therapeutic strategies for pulmonary fibrosis.
- Understanding these pathways may also benefit treatments for fibrosis in other organs, tumors, and aging-related conditions.
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