Research profile

Our research is focused on the cellular and molecular mechanisms of heart dysfunction. The research involves in vivo and in vitro studies of signaling pathways and transcription factors associated with the regulation of cardiomyocyte metabolism and pathogenesis of the left  ventricular hypertrophy, lipotoxic cardiomyopathy and atherosclerosis. In particular, we decipher the mechanisms controlling pericardial and pericoronary adipose tissue function, coronary plaque formation and angiogenesis by functional analysis of stearoyl-CoA desaturase (SCD)-dependent signaling in murine models of lipotoxic heart disease and atherosclerosis. Our second priority is to examine the role of SCD1 and SCD4 genes in coronary atherosclerosis and to determine the role of lipid mediators in cardiomyocyte – pericoronary adipose tissue – endothelial cells communication. We are also interested in mechanisms linking hypoxic cardiomyocytes with angiogenic capacity of endothelial progenitor cells and plasticity of vascular smooth muscle cells. Understanding how hypoxia and lipotoxicity affect vascular homeostasis will not only gain an insight into the basic mechanisms governing vascular biology in health and disease, but it will also provide opportunities for development of new treatment strategies to augment cardiac vascular function and heart remodeling.

Current research activities

• cellular cross-talk between thyroid hormone signaling and lipid mediators in the regulation of heart metabolism and function
• functional role of stearoyl-CoA desaturase in the regulation of angiogenesis in hypoxic cardiac muscle
• role of stearoyl-CoA desaturase in regulation of vascular wall structure in physiology and pathology
• involvement of stearoyl-CoA desaturase-dependent signaling in adipogenesis, secretory function and inflam- mation of pericardial and pericoronary adipose tissue in the healthy heart and in lipotoxic cardiomyopathy and atherosclerosis
• signal transduction and genetic abnormalities in obesity related heart dysfunctions

Selected publications

Bednarski T., Olichwier A., Opasińska A., Pyrkowska A., Gan A.M., Ntambi J.M., Dobrzyń P. (2016) Stearoyl-CoA desaturase 1 deficiency reduces lipid accumulation in the heart by activating lipolysis independently of peroxisome proliferator-activated receptor α. Biochim Biophys Acta-Mol Cell Biol Lipids, 1861: 2029-2037.

Dobrzyń P., Bednarski T., Dobrzyń A. (2015) Metabolic reprogramming of the heart through stearoyl-CoA desaturase. Prog Lipid Res,  57: 1-12.

Dobrzyń P., Pyrkowska A., Duda M., Bednarski T., Mączewski M., Langfort J., Dobrzyń A. (2013) Expression of lipogenic genes is upregulated in the heart with exercise training-induced but not pressure overload-induced left ventricular hypertrophy. Am J Physiol Endocrinol Metab, 304: E1348-E1358.

Dobrzyń P., Dobrzyń A. (2013) Stearoyl-CoA desaturase in the control of heart metabolism. In: Stearoyl-CoA desaturase genes in lipid metabolism J.M. Ntambi (ed.) Springer, New York, 85-101.

Dobrzyń P., Pyrkowska A., Jazurek M., Dobrzyń A. (2012) Increased availability of endogenous and dietary oleic acid contributes to the upregulation of cardiac fatty acid oxidation. Mitochondrion, 12: 132-137.