
In this study, we show that overactivation of CAMK2D underlies the disease phenotype of patients with pathogenic RBM20 variants. What’s more, we could show that this is targetable, and that pharmacological CAMK2 inhibition rescues cardiac dysfunction in a pre-clinical model of RBM20 cardiomyopathy.
Our data position CAMK2D inhibition as the first mechanism-based therapeutic approach for DCM.

To celebrate our successes and have some fun outside the lab, we went bowling and had indian food after. Let's just say, it's good none of us aspired to be a professional bowler :)



Even though Priyanka has only been a year in our lab, she really pushed this project to the finish line. This study is important, because it shows that purely loss-of-function of RBM20 also leads to disease, especially to an increased arrhythmic burden. RBM20 expression modulation, either in RBM20 cardiomyopathy with more severe RS-domain mutation or in cardiometabolic disease to increase compliance of the ventricle, should be carefully considered and monitored.





We have a joined labmeeting with the Beisaw lab, and after labmeeting we had Secret Santa for the first time. A good time was had by all!

Together with the Beisaw lab, on December 9th we visited the Heidelberg Christmas market for some gluhwein and Hot Pot afterwards. Javier (far right) from the Backs lab has been collaborating with us for a long time, and also joined us :).

David's manuscript on sex and gender differences has been accepted at the American Journal of Physiology - Heart and Circulatory Physiology! Congrats, David!
You can find the manuscript here.

On Oct 13th, Zakiya, Fabian, and Maarten visited the EMBL to attend a congress on RBM20 cardiomyopathy