Energy metabolism regulated by HDAC inhibitor attenuates cardiac injury in hemorrhagic rat model.

ABSTRACT: A disturbance of energy metabolism reduces cardiac function in acute severe hemorrhagic patients. Alternatively, adequate energy supply reduces heart failure and increases survival. However, the approach to regulating energy metabolism conductive to vital organs is limited, and the underlying molecular mechanism remains unknown. This study assesses the ability of histone deacetylase inhibitors (HDACIs) to preserve cardiac energy metabolism during lethal hemorrhagic injury. In the lethally hemorrhagic rat and hypoxic myocardial cells, energy metabolism and heart function were well maintained following HDACI treatment, as evident by continuous ATP production with normal cardiac contraction. Valproic acid (VPA) regulated the energy metabolism of hemorrhagic heart by reducing lactate synthesis

SUBMITTER: Kuai Q 

PROVIDER: S-EPMC5133557 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature