Forsøksdyr: Control of cardiomyocyte structure and function by ventricular workload

Godkjenningsdato 04.01.2018

Godkjenningsperiode 04.01.2018-03.01.2022

During heart failure development, the heart is placed under abnormal mechanical load. Our group has observed that increased load is associated with disrupted cell structure and function (Frisk et al., Cardiovasc Res, 2016). T-tubules, critical for ensuring close communication between L-type Ca2+ channels in the surface membrane and ryanodine receptors, are disrupted and disorganized during heart failure. This leads to a weakening of cardiac contraction (Louch et al., J Biomed Biotechnol, 2010). The term “workload” is rather unprecise and our work is focused on precisely dissecting the effects of preload and afterload on cardiomyocyte structure and function, with a particular focus on t-tubules.

The purpose of the project is to better our understanding of how preload and afterload affect t-tubule remodeling during disease, and this knowledge would ultimately potentially aid in the development of novel drug targets to treat heart disease.

For many of the animals that will be used in this project, there will be no harmful effects as they will be euthanized while under anesthesia before any experimentation will be performed. For the animals that will undergo surgical procedures, these animals will develop heart disease over time.

390 animals, rats only, will be used for this project.

Where possible, cells, tissue and data from these animals will be shared with other researchers in order to minimize the use of animals when possible.