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Norwegian University of Science & Technology (NTNU), Faculty of Medicine & Health, Dept. of Circulation & Medical Imaging, Group of Cellular and Molecular Cardiology (GMCC)
Early career investigator (ECI):
Short biography of member:
Dr. Høydal established and head the Group of Molecular and Cellular Cardiology (GMCC) at the department of Circulation and Medical Imaging, Faculty of Medicine, NTNU. Høydal established GMCC with support from the Norwegian Research Council (young research talents) as well as strategic priorities from NTNU, via the Outstanding Academic Fellow program, NTNU. The major aims of Høydal and GMCC is to establish a clinically oriented basic research direction that provides novel insight to the cellular and molecular mechanisms underpinning the transition to heart failure. The major ambition is to establish novel routes to targeted treatment enhance cardiac survival during the process of myocardial infarction as well as treatment of chronic ischemic failing hearts.
The host institution, the Department of Circulation and Medical Imaging, the Faculty of Medicine and Health Sciences (NTNU, Trondheim), offers a unique environment for clinically oriented basic research, with the new integrated university hospital that is "built for multidisciplinary collaboration".
We have established a basic research laboratory with state-of-the-art equipment that is situated under the same roof as the Department of cardiology and cardiothoracic surgery at St. Olavs University Hospital.
The experimental approaches range from whole body characterisation of the heart using testing for aerobic capacity, echocardiography and intraventricular catheterization, to isolated perfused hearts and down to the cellular and molecular mechanisms in isolated cardiomyocytes.
For the characterisation of cellular and molecular mechanisms, we use material from different sources: human cardiac biopsies obtained during surgery, experimental comparative models as well as human Inducible Pluripotent Stem cells (hIPS).
Methodologies include fluorescence microscopy, electrophysiology and confocal imaging in addition to standard technology for molecular regulation by biochemical techniques.
Smenes, B. T. et al. Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial. Interact Cardiovasc Thorac Surg, doi:10.1093/icvts/ivx439 (2018).
Hoydal, M. A. et al. Human cardiomyocyte calcium handling and transverse tubules in mid-stage of post-myocardial-infarction heart failure. ESC Heart Fail, doi:10.1002/ehf2.12271 (2018).
Hoydal, M. A. et al. Exercise training reverses myocardial dysfunction induced by CaMKIIdeltaC overexpression by restoring Ca2+ homeostasis. Journal of applied physiology 121, 212-220, doi:10.1152/japplphysiol.00188.2016 (2016).
Rolim, N. et al. Aerobic interval training reduces inducible ventricular arrhythmias in diabetic mice after myocardial infarction. Basic Res Cardiol 110, 44, doi:10.1007/s00395-015-0502-9 (2015).
Kraljevic, J. et al. Role of KATP Channels in Beneficial Effects of Exercise in Ischemic Heart Failure. Medicine and science in sports and exercise 47, 2504-2512, doi:10.1249/MSS.0000000000000714 (2015).
Slagsvold, K. H., Rognmo, O., Hoydal, M., Wisloff, U. & Wahba, A. Remote ischemic preconditioning preserves mitochondrial function and influences myocardial microRNA expression in atrial myocardium during coronary bypass surgery. Circulation research 114, 851-859, doi:10.1161/CIRCRESAHA.114.302751 (2014).
Slagsvold, K. H. et al. Mitochondrial respiration and microRNA expression in right and left atrium of patients with atrial fibrillation. Physiological genomics 46, 505-511, doi:10.1152/physiolgenomics.00042.2014 (2014).
Slagsvold, K. H. et al. Comparison of left versus right atrial myocardium in patients with sinus rhythm or atrial fibrillation - an assessment of mitochondrial function and microRNA expression. Physiological reports 2, doi:10.14814/phy2.12124 (2014).
Kolseth, S. M. et al. Levosimendan improves contractility in vivo and in vitro in a rodent model of post-myocardial infarction heart failure. Acta physiologica 210, 865-874, doi:10.1111/apha.12248 (2014).
Hoydal, M. A. et al. Reduced aerobic capacity causes leaky ryanodine receptors that trigger arrhythmia in a rat strain artificially selected and bred for low aerobic running capacity. Acta physiologica 210, 854-864, doi:10.1111/apha.12238 (2014).
Kemi, O. J., Haram, P. M., Hoydal, M. A., Wisloff, U. & Ellingsen, O. Exercise training and losartan improve endothelial function in heart failure rats by different mechanisms. Scandinavian cardiovascular journal : SCJ 47, 160-167, doi:10.3109/14017431.2012.754935 (2013).
Johnsen, A. B. et al. Atrial myocyte function and Ca2+ handling is associated with inborn aerobic capacity. PloS one 8, e76568, doi:10.1371/journal.pone.0076568 (2013).
Johnsen, A. B., Hoydal, M., Rosbjorgen, R., Stolen, T. & Wisloff, U. Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure. PloS one 8, e66288, doi:10.1371/journal.pone.0066288 (2013).
Hoydal, M. A. et al. High inborn aerobic capacity does not protect the heart following myocardial infarction. Journal of applied physiology 115, 1788-1795, doi:10.1152/japplphysiol.00312.2013 (2013).
Kolseth, S. M. et al. A dose-response study of levosimendan in a porcine model of acute ischaemic heart failure. European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery 41, 1377-1383, doi:10.1093/ejcts/ezr201 (2012).
Kemi, O. J. et al. Exercise training corrects control of spontaneous calcium waves in hearts from myocardial infarction heart failure rats. Journal of cellular physiology 227, 20-26, doi:10.1002/jcp.22771 (2012).
Kaurstad, G. et al. Chronic CaMKII inhibition blunts the cardiac contractile response to exercise training. European journal of applied physiology 112, 579-588, doi:10.1007/s00421-011-1994-0 (2012).
Koch, L. G. et al. Intrinsic aerobic capacity sets a divide for aging and longevity. Circulation research 109, 1162-1172, doi:10.1161/CIRCRESAHA.111.253807 (2011).
Kemi, O. J. et al. The effect of exercise training on transverse tubules in normal, remodeled, and reverse remodeled hearts. Journal of cellular physiology 226, 2235-2243, doi:10.1002/jcp.22559 (2011).
Leenders, J. J. et al. Regulation of cardiac gene expression by KLF15, a repressor of myocardin activity. The Journal of biological chemistry 285, 27449-27456, doi:10.1074/jbc.M110.107292 (2010).
Gaustad, S. E. et al. Immersion before dry simulated dive reduces cardiomyocyte function and increases mortality after decompression. Journal of applied physiology 109, 752-757, doi:10.1152/japplphysiol.01257.2009 (2010).
Stolen, T. O. et al. Interval training normalizes cardiomyocyte function, diastolic Ca2+ control, and SR Ca2+ release synchronicity in a mouse model of diabetic cardiomyopathy. Circulation research 105, 527-536, doi:10.1161/CIRCRESAHA.109.199810 (2009).
Evensen, K. A. et al. Effects of preterm birth and fetal growth retardation on cardiovascular risk factors in young adulthood. Early human development 85, 239-245, doi:10.1016/j.earlhumdev.2008.10.008 (2009).
Bjorgen, S. et al. Aerobic high intensity one and two legs interval cycling in chronic obstructive pulmonary disease: the sum of the parts is greater than the whole. European journal of applied physiology 106, 501-507, doi:10.1007/s00421-009-1038-1 (2009).
Bye, A. et al. Carbon monoxide levels experienced by heavy smokers impair aerobic capacity and cardiac contractility and induce pathological hypertrophy. Inhalation toxicology 20, 635-646, doi:10.1080/08958370701883821 (2008).
Bye, A. et al. Aerobic capacity-dependent differences in cardiac gene expression. Physiological genomics 33, 100-109, doi:10.1152/physiolgenomics.00269.2007 (2008).
Bye, A. et al. Gene expression profiling of skeletal muscle in exercise-trained and sedentary rats with inborn high and low VO2max. Physiological genomics 35, 213-221, doi:10.1152/physiolgenomics.90282.2008 (2008).
Schroen, B. et al. Lysosomal integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte hypertrophy. The Journal of experimental medicine 204, 1227-1235, doi:10.1084/jem.20070145 (2007).
Kemi, O. J. et al. Exercise training restores aerobic capacity and energy transfer systems in heart failure treated with losartan. Cardiovascular research 76, 91-99, doi:10.1016/j.cardiores.2007.06.008 (2007).
Hoydal, M. A., Wisloff, U., Kemi, O. J. & Ellingsen, O. Running speed and maximal oxygen uptake in rats and mice: practical implications for exercise training. European journal of cardiovascular prevention and rehabilitation : official journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology 14, 753-760, doi:10.1097/HJR.0b013e3281eacef1 (2007).
Hoydal, M. A. et al. Nitric oxide synthase type-1 modulates cardiomyocyte contractility and calcium handling: association with low intrinsic aerobic capacity. European journal of cardiovascular prevention and rehabilitation : official journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology 14, 319-325, doi:10.1097/HJR.0b013e3280128bef (2007).
Hoff, J. et al. Maximal strength training of the legs in COPD: a therapy for mechanical inefficiency. Medicine and science in sports and exercise 39, 220-226, doi:10.1249/01.mss.0000246989.48729.39 (2007).
Care, A. et al. MicroRNA-133 controls cardiac hypertrophy. Nature medicine 13, 613-618, doi:10.1038/nm1582 (2007).
Kemi, O. J. et al. Reduced pH and contractility in failing rat cardiomyocytes. Acta physiologica 188, 185-193, doi:10.1111/j.1748-1716.2006.01621.x (2006).