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- W3012022276 endingPage "547" @default.
- W3012022276 startingPage "509" @default.
- W3012022276 abstract "Oxidative stress has been linked to various disease states as well as physiological aging. The lungs are uniquely exposed to a highly oxidizing environment and have evolved several mechanisms to attenuate oxidative stress. Idiopathic pulmonary fibrosis (IPF) is a progressive age-related disorder that leads to architectural remodeling, impaired gas exchange, respiratory failure, and death. In this article, we discuss cellular sources of oxidant production, and antioxidant defenses, both enzymatic and nonenzymatic. We outline the current understanding of the pathogenesis of IPF and how oxidative stress contributes to fibrosis. Further, we link oxidative stress to the biology of aging that involves DNA damage responses, loss of proteostasis, and mitochondrial dysfunction. We discuss the recent findings on the role of reactive oxygen species (ROS) in specific fibrotic processes such as macrophage polarization and immunosenescence, alveolar epithelial cell apoptosis and senescence, myofibroblast differentiation and senescence, and alterations in the acellular extracellular matrix. Finally, we provide an overview of the current preclinical studies and clinical trials targeting oxidative stress in fibrosis and potential new strategies for future therapeutic interventions. © 2020 American Physiological Society. Compr Physiol 10:509-547, 2020." @default.
- W3012022276 created "2020-03-23" @default.
- W3012022276 creator A5009964667 @default.
- W3012022276 creator A5056909095 @default.
- W3012022276 creator A5059451166 @default.
- W3012022276 creator A5081550304 @default.
- W3012022276 date "2020-03-12" @default.
- W3012022276 modified "2023-10-14" @default.
- W3012022276 title "Oxidative Stress in Pulmonary Fibrosis" @default.
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