OPN is highly induced in CNT-exposed lungs and plays critical roles in TGF-β1 signaling activation and myofibroblast differentiation to promote fibrosis development from MWCNT exposure. This study reveals an OPN-dependent mechanism to promote MWCNT-induced lung fibrosis. The findings raise the possibility of using OPN as a biomarker to monitor CNT exposure and as a drug target to halt fibrosis development.
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Dong et al. (2017) studied this question.
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