Rate My Professor Coen Ottenheijm

Coen Ottenheijm, PhD, serves as Associate Professor in the Department of Cellular and Molecular Medicine at The University of Arizona, where he leads the Ottenheijm Laboratory within the Molecular Cardiovascular Research Program. He earned his PhD in 2006 from the Department of Pulmonology at Radboud University Nijmegen Medical Center in the Netherlands, investigating diaphragm muscle dysfunction in patients with chronic lung disease. Subsequently, he completed a postdoctoral fellowship in the laboratory of Dr. Henk Granzier at The University of Arizona, funded by an NWO Rubicon grant, focusing on sarcomere proteins including titin and nebulin, and developing the first nebulin knockout mouse model mimicking nemaline myopathy. His research expertise lies in the pathophysiology of diaphragm weakness in critically ill patients, particularly during mechanical ventilation in the intensive care unit. The Ottenheijm Laboratory employs genetically engineered mouse models, diaphragm biopsies from ICU patients, single muscle fiber mechanics, proteomics, transcriptomics, and high-resolution microscopy to elucidate molecular mechanisms, with a special emphasis on titin as a giant mechanosensor protein regulating diaphragm contractility.

Ottenheijm's contributions have significantly advanced the understanding of ventilator-induced diaphragm dysfunction and potential therapeutic interventions. He received a $2.3 million grant from the National Institutes of Health to study titin's role in diaphragm weakness during mechanical ventilation. His laboratory tests novel therapeutics, such as troponin activators, to enhance diaphragm muscle fiber strength in patient samples. Ottenheijm has authored over 120 peer-reviewed publications, achieving an h-index of 44 and more than 5,500 citations per Google Scholar. Key publications include 'Triggering typical nemaline myopathy with compound heterozygous nebulin mutations reveals myofilament structural changes as pathomechanism' (Nature Communications, 2020), 'Downsizing the molecular spring of the giant protein titin reveals that skeletal muscle titin determines passive stiffness and drives longitudinal hypertrophy' (eLife, 2018), 'Diaphragm Atrophy and Weakness in the Absence of Mitochondrial Dysfunction in the Critically Ill' (American Journal of Respiratory and Critical Care Medicine, 2017), and 'Unaffected contractility of diaphragm muscle fibers in humans on mechanical ventilation' (American Journal of Physiology - Lung Cellular and Molecular Physiology, 2014). His work informs strategies to mitigate weaning failure and mortality in ICU settings.