Ischemic heart disease is the main cause of mortality worldwide. We study cardiac tolerance to injury caused by acute oxygen deprivation from the molecular level to the whole organism using animal models. Our research is focused mainly on the study of mechanisms that underlie:
- high cardiac tolerance to injury early ontogeny,
- increased cardiac tolerance induced by adaptation to chronic hypoxia and regular exercise training,
- permanent consequences of early developmental interventions for cardiac tolerance in adulthood,
- and altered cardiac tolerance associated with various pathological states.
Further we study heart development with special emphasis on the cardiac conduction system. Our current research is focused on the following projects:
- elucidating cardiac conduction system formation with phylogenetic approaches,
- dynamic imaging methods for cardiac conduction system,
- and development of new methods for quantitative analysis of fibrous structures to study branching patterns of the coronary vessels and cardiac conduction system.
13th conference New Frontiers in Basic Cardiovascular Research
Projects
This projects aims to obtain new insights into cardiac conduction system formation through comparative morphological and physiological approach.
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The immature heart is highly tolerant to ischemic injury, but chronic oxygen deficit during early ontogeny may have negative consequences that persist till adulthood. We study mechanisms responsible for developmental changes of cardiac ischemic tolerance.
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Systemic hypertension is a major risk factor of ischemic heart disease. However, it can also stimulate mechanisms that protect the heart against acute oxygen deprivation. We study the effects of various forms of hypertension on cardiac ischemic tolerance.
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Prolonged exposure to hypoxic environment leads to adaptation which is associated with improved cardiac tolerance to acute oxygen deprivation. We study molecular mechanisms underlying the cardioprotective effects of chronic hypoxia on various manifestations of ischemic injury.
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Publications
Semenzato; M. - Kohr; M. J. - Quirin; Ch. - Menab?; R. - Alánová; Petra - Alán; L. - Pellattiero; A. - Murphy; E. - Di Lisa; F. - Scorrano; L.
Oxidization of optic atrophy 1 cysteines occurs during heart ischemia-reperfusion and amplifies cell death by oxidative stress
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Redox Biology. 2023; 63(July)); 102755
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IF = 11.4
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Ošťádal; Bohuslav - Kolář; František - Ošťádalová; Ivana - Sedmera; David - Olejníčková; Veronika - Hlaváčková; Markéta - Alánová; Petra
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Developmental Aspects of Cardiac Adaptation to Increased Workload
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Journal of cardiovascular development and disease. 2023; 10(5)); 205
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IF = 2.4
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Husková; Z. - Kikerlová; S. - Miklovič; M. - Kala; P. - Papoušek; František - Neckář; Jan
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Inappropriate activation of the renin-angiotensin system improves cardiac tolerance to ischemia/reperfusion injury in rats with late angiotensin II-dependent hypertension
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Frontiers in Physiology. 2023; 14(14 June)); 1151308
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IF = 4.0
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Benák; Daniel - Kolář; František - Zhang; L. - Devaux; Y. - Hlaváčková; Markéta
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RNA modification m6Am: the role in cardiac biology
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Epigenetics. 2023; 18(1); 2218771
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IF = 3.7
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Benák; Daniel - Benáková; Štěpánka - Plecitá-Hlavatá; Lydie - Hlaváčková; Markéta
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The role of m6A and m6Am RNA modifications in the pathogenesis of diabetes mellitus
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Frontiers in Endocrinology. 2023; 14(July); 1223583
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IF = 5.2
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