Executive Summary : | Cardiovascular diseases are a major cause of death, causing 17.9 million deaths annually and 32% of all deaths worldwide. Ischaemia/reperfusion injury is a common pathology in CVD, and long-term cardiac management becomes more challenging after COVID-19. Lower vertebrates, such as zebrafish, newts, and axolotls, have demonstrated remarkable ability in heart regeneration. This phenomenon remains enigmatic, but zebrafish has emerged as a well-established model to study cardiac remodeling after injury. The post-injury scar of zebrafish hearts can be replaced by newly formed cardiomyocytes, which are regulated by factors such as PCNA expression, phosphor histone-H3, and regeneration markers like tcf21, pdgf a, pdgf b, vegf, neuregulin1, and anti-apoptotic factors. Endocrine control of regenerative tissues is a great interest in regenerative medicine. Teleost vertebrates lack an organized and compact thyroid gland, but they bear dispersed thyroid follicles in clusters around the basibranchial region. Thyroid hormone receptors (TRs) are nuclear receptors that regulate physiological, cellular, and developmental functions in vertebrate hearts. Thyroid hormone control of cardiomyocyte re-entering the cell cycle during cardiac tissue regeneration is evident, but the molecular pathways are still a matter of conjecture. The proposed project aims to identify molecular pathways involved in thyroid hormone regulation in the rate of heart regeneration in an anaemic hypoxia-reoxygenation model of zebrafish by modulating thyroid receptor actions in different experimental points. |