Morten Høydal
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
- (2021) Acute high-intensity aerobic exercise increases gene expression of calcium-related proteins and activates endoplasmic reticulum stress responses in diabetic hearts. Comparative Exercise Physiology. vol. 17 (2).
- (2020) Exercise training reveals micro-RNAs associated with improved cardiac function and electrophysiology in rats with heart failure after myocardial infarction. Journal of Molecular and Cellular Cardiology. vol. 148.
- (2019) High intensity interval training ameliorates mitochondrial dysfunction in the left ventricle of mice with type 2 diabetes. Cardiovascular Toxicology. vol. 19 (5).
- (2019) microRNA-451a prevents activation of matrix metalloproteinases 2 and 9 in human cardiomyocytes during pathological stress stimulation. American Journal of Physiology - Cell Physiology. vol. 318 (1).
- (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).
- (2019) Effect of exercise training on cardiac metabolism in rats with heart failure. Scandinavian Cardiovascular Journal.
- (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.
- (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).