Journal
ANTIOXIDANTS & REDOX SIGNALING
Volume 10, Issue 2, Pages 343-354Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2007.1908
Keywords
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Funding
- NHLBI NIH HHS [R01 HL063700, R01 HL063700-07, R01 HL63700] Funding Source: Medline
- NIDCR NIH HHS [R01 DE016226-01] Funding Source: Medline
- NIEHS NIH HHS [R21 ES013986, F32 ES015383, F32 ES015383-01] Funding Source: Medline
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Disruption of the oxidant/antioxidant balance in the lung is thought to be a key step in the development of many airway pathologies. Hence, antioxidant enzymes play key roles in controlling or preventing pulmonary diseases related to oxidative stress. The superoxide dismutases ( SOD) are a family of enzymes that play a pivotal role protecting tissues from damage by oxidant stress by scavenging superoxide anion, which prevents the formation of other more potent oxidants such as peroxynitrite and hydroxyl radical. Extracellular SOD (EC-SOD) is found predominantly in the extracellular matrix of tissues and is ideally situated to prevent cell and tissue damage initiated by extracellularly produced ROS. EC-SOD has been shown to be protective in several models of interstitial lung disease, including pulmonary fibrosis. In addition, alterations in EC-SOD expression are also present in human idiopathic pulmonary fibrosis (IPF). This review discusses EC-SOD regulation in response to pulmonary fibrosis in animals and humans and reviews possible mechanisms by which EC-SOD may protect against fibrosis.
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