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Updated: Dec 24, 2025

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Linking cellular energy state to atrial fibrillation pathogenesis: Potential role of adenosine
Praloy Chakraborty1, Stanley Nattel2, Kumaraswamy Nanthakumar1
1Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada; University Health Network, Toronto, Ontario, Canada.
Abstract:
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.
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