Search for: [Abstract = "at PF543 administration partially protected against left ventricular hypertrophy in response to AngII treatment. PF543 significantly downregulated the expression of hypertrophy markers as examined by transcriptomic analysis, whereas histological analysis revealed that the inhibitor prevented cardiomyocyte enlargement, while it had no effect on cardiac fibrosis in hypertensive animals. The mechanism of PF543 action could be mediated by decreased S1pr1 expression, as well as by upregulated levels of S1P precursors, and this was accompanied by the inhibition of signaling pathways involving Rock1, PKC, Erk1\/2 and Stat3. The thesis also aimed to assess the effects of siRNA\-induced Sphk1 deficiency on the development of hypertrophy in mouse neonatal cardiomyocytes in vitro. Interestingly, downregulation of Sphk1 did not affect biological pathways related to the pathological type of hypertrophy, while it induced molecular pathways promoting final differentiation of cardiomyocytes at postnatal stage. Promotion of pathways characteristic for cardiomyocyte maturation was associated with the activation or upregulated expression of Akt and Mkk4 kinases, respectively. In summary, the studies described in this thesis found that PF543 inhibitor acted as an agent partially preventing cardiac hypertrophy and improving endothelial function in AngII\-induced hypertension in mice. Additionally, th"]

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