作者
Srikanth Perike,Francisco J. González-González,Issam Abu-Taha,Frederick W. Damen,Laurin M. Hanft,Ken S. Lizama,Anahita Aboonabi,Andrielle Elaine Capote,Yuriana Aguilar-Sánchez,Benjamin S. Levin,Zhenbo Han,Arvind Sridhar,Jacob Grand,Joel W. Martin,Joseph G. Akar,Chad M. Warren,R. John Solaro,Sang‐Ging Ong,Dawood Darbar,Kerry S. McDonald,Craig J. Goergen,Beata M. Wolska,Dobromir Dobrev,Xander H.T. Wehrens,Mark McCauley
摘要
Atrial fibrillation (AF)-the most common sustained cardiac arrhythmia-increases thromboembolic stroke risk 5-fold. Although atrial hypocontractility contributes to stroke risk in AF, the molecular mechanisms reducing myofilament contractile function remain unknown. We tested the hypothesis that increased expression of PPP1R12C (protein phosphatase 1 regulatory subunit 12C)-the PP1 (protein phosphatase 1) regulatory subunit targeting MLC2a (atrial myosin light chain 2)-causes hypophosphorylation of MLC2a and results in atrial hypocontractility.