Linking cellular energy state to atrial fibrillation pathogenesis: Potential role of adenosine monophosphate-activated protein kinase.
Adenosine monophosphate-activated protein kinase (AMPK) is the cellular stress-sensing molecule. Apart from maintaining cellular energy balance, AMPK controls expression and regulation of ion channels and ion transporters, including cytosolic Ca2+ handling proteins. Emerging evidence suggests that metabolic impairment plays a crucial role in the pathogenesis of atrial fibrillation. AMPK activation is thought to be protective by preventing metabolic stress, favorably modulating membrane electrophysiology including cytosolic Ca2+ dynamics; preventing cellular growth; and hypertrophic remodeling. This review considers current concepts and evidence from clinical and experimental studies regarding the role of AMPK in atrial fibrillation.
['Chakraborty|Praloy|P|', 'Nattel|Stanley|S|', 'Nanthakumar|Kumaraswamy|K|']
D055372:AMP-Activated Protein Kinases D000818:Animals D001281:Atrial Fibrillation D002118:Calcium D002478:Cells, Cultured D004734:Energy Metabolism D006801:Humans D013312:Stress, Physiological
AMPK AF CaTs DAD