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Group of muscle physiology and cold acclimation signaling

Maintaining energy homeostasis is essential for the proper function of all tissues, including the heart. Serious disruption of energy homeostasis during ischemic states may lead to cell death activation and can damage cardiac function. The subsequent restoration of flow is essential, yet causes excessive oxidative stress which further damages affected tissue. Cellular resistance to ischemic/reperfusion damage may be increased through various interventions which activate the cell’s endogenous protective mechanisms. These include for example, physical exertion, adaptation to chronic hypoxia, preconditioning, and the effect of thyroidal hormones or cold. Study of the nature of endogenous protective mechanisms is important to improve our understanding of these processes, which may be used to prevent and treat cardiovascular disease. Our laboratory focuses on studying the following three models:

         The effect of cold adaptation on the cardiovascular system, protective and detrimental effects. The effect of cold exposure on cardiac sensitivity to ischemic/reperfusion damage and on cardiac function. At the cellular level, monitoring the effect of thyroid conditions on the heart, mitochondrial function, oxidative stress, cell death and its related signal pathways. In cooperation with Prof. F. Kolář (Dept. of Developmental Cardiology, CAS Institute of Physiology) and Dr. P. Flachs (Dept. of Fat Tissue Biology, CAS Institute of Physiology).


Head: doc. RNDr. Jitka Žurmanová, PhD. (E-mail: jitka.zurmanova@natur.cuni.cz, tel. 221951790)
Laboratory: Viničná 7, 1st basement, door no. S39

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