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Pathophysiological Consequences of TAT-HKII Peptide Administration Are Independent of Impaired Vascular Function and Ensuing Ischemia

Previously, we demonstrated the benefit of the glycolytic enzyme hexokinase (HK) binding to mitochondria during ischaemic preconditioning, and that disrupting this binding with a targeted peptide damages heart function. However, it has been postulated that the peptide that disrupts this binding causes cardiac dysfunction by vasoconstriction and ischaemia rather than disrupting of HK-mitochondrial binding. In this paper we showed this was not the case and confirmed our hypothesis that HK-mitochondrial association is essential for normal cardiac function, and augmenting it is a new strategy for cardiac protection. Southworth performed the electron microscopic analysis, jointly the data analysis and manuscript preparation.