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Stress-activated kinase MKK7 governs epigenetics of cardiac repolarisation for arrhythmia prevention
Over half of heart failure patients die of arrhythmic death, which claims about 20% of total mortalities worldwide, and 100,000 lives a year in UK, more than breast cancer, lung cancer and AIDS combined. Current anti-arrhythmic agents are designed to block ion channel activity, which can cause pro-arrhythmic effects, culminating in greater overall mortality risk. Our current work provides important evidence supporting an emerging concept by targeting “upstream regulators” of ion channels as a new treatment route against ventricular arrhythmias. We recently discovered a novel mechanism underlying gene regulation of a set of potassium (K+) channels through a signalling complex comprised of mitogen-activated kinase kinase 7 (MKK7), histone deacetylase 2 (HDAC2) and Krϋppel-like factor 4 (KLF4). Gain and loss of function studies demonstrate a critical link of stress signalling pathways through the MKK7/HDAC2/KLF4 mechanism with repression of cardiac K+ channels, repolarisation delay and susceptibility to arrhythmias. Our data in an arrhythmic mouse model further reveal the effect of HDAC2 inhibition by pharmacological inhibitors on restoring K+ activity and reducing arrhythmic propensity. This study suggests a gene regulatory avenue for treatment of cardiac arrhythmias.
Date:
16 October 2015, 12:00
Venue:
Sherrington Building, off Parks Road OX1 3PT
Venue Details:
Cardiac Seminar Room
Speaker:
Dr Xin Joy Wang (University of Manchester, Faculty of Life Sciences)
Organising department:
Department of Physiology, Anatomy and Genetics (DPAG)
Organiser:
Dr Vicki Dunn (University of Oxford)
Organiser contact email address:
paterson-pa@dpag.ox.ac.uk
Host:
Professor David Paterson (University of Oxford)
Booking required?:
Not required
Audience:
Members of the University only
Editor:
Vicki Dunn
