High Sensitivity of SIRT3 Deficient Hearts to Ischemia-Reperfusion Is Associated with Mitochondrial Abnormalities.

ABSTRACT: Aim: Sirtuins are NAD⁺-dependent deacetylases that regulate cell metabolism through protein acetylation/deacetylation, and SIRT3 is the major deacetylase among mitochondrial isoforms. Here, we elucidated the possible role of acetylation of cyclophilin D, a key regulator of the mitochondrial permeability transition pore (mPTP), in mitochondria-mediated cardiac dysfunction induced by ischemia-reperfusion (IR) in wild type (WT) and SIRT3 knockout (SIRT3^-/-) mice. Materials and Methods: Isolated and Langendorff-mode perfused hearts of WT and SIRT3^-/- mice were subjected to 25-min global ischemia followed by 60-min of reperfusion in the presence or absence of the mPTP inhibitor, sanglifehrin A (SfA). Results: Analysis of mitochondrial sirtui

SUBMITTER: Parodi-Rullan RM 

PROVIDER: S-EPMC5432544 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature