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. Author manuscript; available in PMC: 2009 Mar 25.
Published in final edited form as: Antioxid Redox Signal. 2008 Feb;10(2):355–370. doi: 10.1089/ars.2007.1916

FIG. 1. Role of ROS in the dysregulation of tissue repair.

FIG. 1

Several phosphatases contain sensitive thiol residues that are inhibited on oxidation. As steady-state levels of oxidants increase, an increase in the inactivation of phosphatases and a corresponding increase in the levels and duration of phosphorylated proteins occur. An increase in steady-state ROS results in altering the cellular glutathione (GSH)/glutathione disulfide (GSSG) redox couple, which can in turn alter the relative oxidation status of protein thiols. In addition, ROS can alter cell signaling directly by reacting with specific thiols on transcription factors. Many of these types of mechanisms are thought to contribute to the often observed unregulated tissue-repair responses associated lung fibrosis.