Paul Wijnker is a Postdoctoral researcher at the Department of Physiology, Amsterdam Cardiovascular Sciences, at the Amsterdam UMC.
Dr Wijnker is fascinated by the multiple mechanisms that affect muscle contractility in health and disease. He obtained a PhD degree in Medical Sciences from the VU University in Amsterdam. During his PhD, he optimized a troponin exchange method and contributed greatly to the understanding of consequences of site-specific phosphorylation of cardiac troponin I in human cardiomyocytes, which is changed in heart failure. He also contributed to the discovery of a new common finding in human hypertrophic cardiomyopathy (HCM) muscle - impaired length-dependent activation, and revealed HCM gene-specific perturbations of myofilament function. He then worked at the Department of Experimental Pharmacology and Toxicology, Cardiovascular Research Center, at the University Medical Center Hamburg-Eppendorf (UKE) in Germany. At the UKE, he revealed direct effects of different types of HCM mutations on cardiac contractility in mouse engineered heart tissue (EHT). The focus of his current research is on molecular alterations and treatment targets for HCM in a human cardiac disease model (EHT), which he has set up at the Department of Physiology in Amsterdam. He recently generated human EHT harboring different HCM gene mutations and investigates mutation-specific effects on contractility of the heart and mutation-specific therapies.