16/06/2016
In a new study Elkouris et al. demonstrate that Set9 methyltransferase function is required for the development of pulmonary fibrosis in mice. The mechanism involves Set9-mediated methylation of Smad7, the inhibitory component of the TGF-β signaling pathway. Methylation promotes Smad7 degradation and facilitates TGF-β-dependent activation of extracellular matrix genes. Genetic ablation or pharmacological inhibition of Set9 greatly impaired experimentally induced lung fibrosis in mouse models.