Cardiac Rac1 overexpression in mice creates a substrate for atrial arrhythmias characterized by structural remodelling

Abstract

The substrate for atrial arrhythmias in mice with Rac1 overexpression is characterized by conduction disturbances and atrial fibrosis. Electrical remodelling (i.e. a shortening of AERP) does not play a role. Statin treatment cannot prevent the structural and electrophysiological effects of pronounced Rac1 overexpression in this model.

ATP-binding cassette transporter Abcg2 lineage contributes to the cardiac vasculature after oxidative stress

“…This chemical was chosen as a simple and effective agent for generating cellular oxidative stress levels without concomitant tissue injury. To date, there has not been a suitable alternative for an in vivo oxidative stress model without tissue injury (1,3,6,8,12,29,32,38). As reported in previous studies (2, 4) using PQ to generate high-level ROS to mimic disease systems, we observed a significant increase in oxidative stress markers in cardiac tissue within hours of treatment.…”

Mutation of the Calmodulin Binding Motif IQ of the L-type Cav1.2 Ca2+ Channel to EQ Induces Dilated Cardiomyopathy and Death

“…Simultaneous Calcium and Electrophysiological RecordingsRecordings were performed as described earlier (28). For assessing the EC coupling gain we followed a protocol described in Ref.…”

HDAC4 controls histone methylation in response to elevated cardiac load

“…Conditional mutant mice with cardiac-specific Hdac4 deletion were generated by crossing existing Working heart experiments. Working heart experiments were performed as described previously (42). Briefly, hearts were perfused with Krebs-Henseleit solution at 37°C in a Langendorff apparatus, paced at 400 bpm, and exposed to effective preload of 10 mmHg and afterload of 80 mmHg.…”