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AECs in the lungs produce catalase, which exerts its activity via reducing H 2 O 2 and, therefore, inhibits H 2 O 2 -mediated fibroblast activation in IPF lungs (Waghray et al., 2005)

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It promotes the production and release of inflammatory mediators, while the inflammatory response conversely exacerbates oxidative stress, forming a vicious cycle 5