Morten Høydal
Researcher and head of GMCC (Group of Cellular and Molecular Cardiology)
Department of Circulation and Medical Imaging Faculty of Medicine and Health SciencesBackground and activities
Diseases affecting the heart are characterized by the activation of a variety of intracellular signaling pathways and transcriptional mediators that causes breakdown of cardiac function, pathological remodeling as well as triggering of lethal cardiac arrhythmias.
My aim is to establish a clinical oriented basic research direction for developing new therapeutic strategies for heart failure based on a better understanding of the underlying cellular and molecular mechanisms of the disease.
The specific objective of my research is to form the basis for developing new therapeutic strategies for heart failure based on the hypothesis that altered regulation of a new class of non-coding RNA, microRNA, causes post- transcription repression or mRNA degradation of key proteins involved in cardiomyocyte excitation-contraction-coupling, Calcium homeostasis and electrical properties in the failing heart.
Publications listed in publication databases
PubMed
Scientific, academic and artistic work
A selection of recent journal publications, artistic productions, books, including book and report excerpts. See all publications in the database
Journal publications
- (2019) The effect of exercise training on myocardial and skeletal muscle metabolism by MR spectroscopy in rats with heart failure. Metabolites. vol. 9:53 (3).
- (2018) Human cardiomyocyte calcium handling and transverse tubules in mid-stage of post-myocardial-infarction heart failure. ESC Heart Failure. vol. 5 (3).
- (2018) Skeletal muscle metabolism in rats with low and high intrinsic aerobic capacity: Effect of aging and exercise training. PLOS ONE. vol. 13 (12).
- (2018) Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial. Interactive Cardiovascular and Thoracic Surgery. vol. 27 (1).
- (2017) Acute exhaustive aerobic exercise training impair cardiomyocyte function and calcium handling in Sprague-Dawley rats. PLOS ONE. vol. 12 (3).
- (2017) Modeling of cardiac ischaemia and reperfusion injury: a human-based in vitro model using iPS-derived cardiomyocytes. European Heart Journal. vol. 38 (1).
- (2017) MicroRNA-451a regulate expression and activity of matrix metalloproteinases 2 and 9 in human cardiomyocytes. European Heart Journal. vol. 38 (1).
- (2016) Exercise training reverses myocardial dysfunction induced by CaMKIIC overexpression by restoring Ca2+ homeostasis. Journal of applied physiology. vol. 121 (1).
- (2015) Role of KATP channels in beneficial effects of exercise in ischemic heart failure. Medicine & Science in Sports & Exercise. vol. 47 (12).
- (2015) Aerobic interval training reduces inducible ventricular arrhytmias in diabetic mice after myocardial infarction. Basic Research in Cardiology. vol. 110 (44).
- (2014) 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. vol. 210 (4).
- (2014) Levosimendan improves contractility in vivo and in vitro in a rodent model of post-myocardial infarction heart failure. Acta Physiologica. vol. 210 (4).
- (2014) 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. vol. 2 (e12124).
- (2014) Mitochondrial respiration and microRNA expression in right and left atrium of patients with atrial fibrillation. Physiological Genomics. vol. 46 (14).
- (2014) Remote ischemic preconditioning preserves mitochondrial function and activates pro-survival protein kinase Akt in the left ventricle during cardiac surgery: A randomized trial. International Journal of Cardiology. vol. 177 (2).
- (2014) Remote ischemic preconditioning preserves mitochondrial function and influences myocardial MicroRNA expression in atrial myocardium during coronary bypass surgery. Circulation Research. vol. 114 (5).
- (2013) High inborn aerobic capacity does not protect the heart following myocardial infarction. Journal of applied physiology. vol. 115 (12).
- (2013) Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure. PLOS ONE. vol. 8 (6:e66288).
- (2013) Atrial Myocyte Function and Ca2+ Handling Is Associated with Inborn Aerobic Capacity. PLOS ONE. vol. 8 (10).
- (2013) Exercise training and losartan improve endothelial function in heart failure rats by different mechanisms. Scandinavian Cardiovascular Journal. vol. 47 (3).