Tsushima, Robert G.Anser, Fahad2024-03-182024-03-182024-03-16https://hdl.handle.net/10315/41887Syntaxin-1A (STX1A) is a member of the SNARE family which is recognized for its role in membrane exocytosis and ion-channel regulation. Although the physiological properties of STX1A has been assessed in many tissues, its role within the heart remains unelucidated. To address this, a cardiomyocyte specific STX1A knockout (KO) model was generated in adult C57BL/6J mice. Through utilization of both in vivo and in vitro approaches, STX1A haploinsufficiency was demonstrated to induce transient contractile dysfunction, a global electromechanical delay, and reduction in Ca2+ handling gene expression. The depressed cardiac function was supported by volumetric overload of the left-ventricle and cardiomyocyte/sarcomeric restructuring. Furthermore, pathological hypertrophy was observed as evident by the re-expression of fetal genes and left-ventricular fibrosis. Collectively, the results suggest an important role of STX1A in cardiac E-C coupling, whereby its KO impairs the heart’s electromechanical function and induces ventricular remodelling to compensate for the elevated hemodynamic volume overload.Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.BiologyPhysiologyElectronic Thesis or Dissertation2024-03-16SNAREsSTX1ACardiacHypertrophyHeart failure