Journal
ANTIOXIDANTS & REDOX SIGNALING
Volume 10, Issue 2, Pages 355-370Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2007.1916
Keywords
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Funding
- NHLBI NIH HHS [R01 HL075523, R01 HL75523, R01 HL075523-01, R01 HL084469-02, R01 HL075523-04, R01 HL084469, R01 HL075523-03, R01 HL075523-02, R01 HL084469-01A2] Funding Source: Medline
- NIEHS NIH HHS [U54 ES015678-010002, R01 ES012504-02, R01 ES017582, U54 ES015678, R01 ES012504-03S1, R01 ES012504, U54 ES015678-020002, R01 ES012504-01, R01 ES012504-03, R01 ES012504-04, U54 ES015678-030002] Funding Source: Medline
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Interstitial lung disease encompasses a large group of chronic lung disorders associated with excessive tissue remodeling, scarring, and fibrosis. The evidence of a redox imbalance in lung fibrosis is substantial, and the rationale for testing antioxidants as potential new therapeutics for lung fibrosis is appealing. Current animal models of lung fibrosis have clear involvement of ROS in their pathogenesis. New classes of antioxidant agents divided into catalytic antioxidant mimetics and antioxidant scavengers are being developed. The catalytic antioxidant class is based on endogenous antioxidant enzymes and includes the manganese-containing macrocyclics, porphyrins, salens, and the non-metal-containing nitroxides. The antioxidant scavenging class is based on endogenous antioxidant molecules and includes the vitamin E analogues, thiols, lazaroids, and polyphenolic agents. Numerous studies have shown oxidative stress to be associated with many interstitial lung diseases and that these agents are effective in attenuating fibroproliferative responses in the lung of animals and humans.
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