Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
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.
