Rate My Professor Henk Granzier

Granzier's research investigates the giant elastic protein titin, spanning the half-sarcomere from Z-disk to M-band, and its roles as a molecular spring, mechanosensor, and regulator of myocardial passive stiffness, sarcomere length, thick filament length, and calcium sensitivity in striated muscle. His laboratory employs bioengineering, physiology, and mechanical approaches, including mouse models with targeted titin modifications such as deletions in spring elements, PEVK region, and IA-junction, to elucidate mechanisms in heart function, Frank-Starling response, diastolic dysfunction, heart failure with preserved ejection fraction, dilated cardiomyopathy, nemaline myopathy, and nebulin-related disorders. Key publications include "Folding-unfolding transitions in single titin molecules characterized with laser tweezers" (Science, 1997), "Myocardial stiffness in patients with heart failure and a preserved ejection fraction: contributions of collagen and titin" (Circulation, 2015), "Deleting titin's I-band/A-band junction reveals critical roles for titin in biomechanical sensing and cardiac function" (PNAS, 2014), and "Discovery of Titin and Its Role in Heart Function and Disease" (Circulation Research, 2025). With over 205 publications, his pioneering work on titin biomechanics, isoforms, posttranslational modifications like phosphorylation, and single-molecule techniques has profoundly influenced the field. Honors include the Henry and Phyllis Koffler Prize (2023), UArizona Founders Day honoree (2024), Helmholtz-Humboldt Research Award (2006), Pfizer Award for Research Excellence (2005), American Heart Association Established Investigator (2000), and Elected Associate Editor of Circulation: Heart Failure (2017).