Atrial fibrillation (AF) is is associated with an atrial arrhythmogenic substrate comprised of electrical, structural, and Ca2+-handling remodeling that supports the induction and maintenance of the arrhythmia. We have recently discovered increased atrial NLRP3-inflammasome related signaling as a unifying principle for the development and persistence of AF-related atrial remodeling. New-onset AF has been identified as a frequent complication of reperfused ventricular myocardial infarction.

 

To identify the underlying molecular and cellular mechanisms that promote the evolution and maintenance of an atrial arrhythmogenic substrate after ventricular myocardial infarction with a focus on: 

• Atrial NLRP3-inflammasome activity and regulation
• Atrial cardiomyocyte ion channel and calcium-handling alterations
• Atrial MultiOmics and structural remodeling
• Atrial (epi)genetics and transcriptional remodeling
• Functional consequences of ischemia-related atrial remodeling 
• Therapeutic targeting of ischemia-related atrial remodeling

 

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In vitro and in vivo phenotyping of atrial function

 

Principal Investigators

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