Mattias F. Lindberg

The paper develops a computational network model predicting DYRK1A inhibition promotes cardiomyocyte cycling after ischemic/reperfusion injury, validated through experiments in neonatal rat cardiomyocytes.

This study shows that CILK1 accumulates in an inactive form during ADPKD progression in human and mouse models.

This study shows that Leucettinib-21 reduces DYRK1A activity in human trisomy 21 neural cells, supporting its potential as a therapeutic for Down syndrome.