This study investigates the development of heart failure with reduced ejection fraction and its relationship with coronary microcirculation. Mice model with adipose specific overexpression of Triadin was utilized to perform 2-D Echocardiography, strain echocardiography, coronary microcirculation/perfusion evaluation. Molecular analysis was performed to study the role of SIRT1, adrenergic receptors, calcium signallling genes in the development of HFrEF phenotype. Another transgenic strain (5XFAD) was used to study the role of beta amyloids and human amyloid precursor protein in the development of HFrEF. Coronary and cerebral microcirculation was evaluated as well. Molecular mechanisms were evaluated to study the role of beta amyloids/human amyloid precursor protein in impairment of autophagy. In conclusion, this study attempts to perform phenotypic characterization of different transgenic mice models of heart failure with reduced ejection fraction through 2-D, strain echocardiography, laser speckle contrast imaging (for coronary microcirculation evaluation) and investigation of the underlying dysfunctional molecular mechanisms.
