This study elucidates a specific molecular pathway (Arkadia-mediated Smad7 degradation via Ang II/AT1 receptor activation) responsible for atrial fibrosis in the setting of atrial fibrillation.
Ang II/AT(1) receptor-specific activation of Arkadia-mediated poly-ubiquitination and degradation of Smad7 may decrease the inhibitory feedback regulation of TGF-β(1)/Smad signaling and serves as a key mechanism for AF-induced atrial fibrosis.
He et al. (2010) studied this question.