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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Koentges, C; Pfeil, K; Meyer-Steenbuck, M; Lother, A; Hoffmann, MM; Odening, KE; Hein, L; Bode, C; Bugger, H.
Preserved recovery of cardiac function following ischemia-reperfusion in mice lacking SIRT3.
Can J Physiol Pharmacol. 2016; 94(1): 72-80. Doi: 10.1139/cjpp-2015-0152
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Führende Autor*innen der Med Uni Graz
Bugger Heiko Matthias
Co-Autor*innen der Med Uni Graz
Pfeil Katharina
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Abstract:
Lack of the mitochondrial deacetylase sirtuin 3 (SIRT3) impairs mitochondrial function and increases the susceptibility to induction of the mitochondrial permeability transition pore. Because these alterations contribute to myocardial ischemia-reperfusion (IR) injury, we hypothesized that SIRT3 deficiency may increase cardiac injury following myocardial IR. Hearts of 10-week-old mice were perfused in the isolated working mode and subjected to 17.5 min of global no-flow ischemia, followed by 30 min of reperfusion. Measurements before ischemia revealed a decrease in cardiac power (-20%) and rate pressure product (-15%) in SIRT3(-/-) mice. Mitochondrial state 3 respiration (-15%), ATP synthesis (-39%), and ATP/O ratios (-29%) were decreased in hearts of SIRT3(-/-) mice. However, percent recovery of cardiac power (WT 94% ± 9%; SIRT3(-/-) 89% ± 9%) and rate pressure product (WT 89% ± 16%; SIRT3(-/-) 96% ± 3%) following IR was similar in both groups. Myocardial infarct size was not increased in SIRT3(-/-) mice following permanent ligation of the left anterior descending coronary artery (LAD). Left ventricular pressure and dP/dtmax, and mitochondrial respiration and ATP synthesis were not different between groups following LAD ligation. Thus, despite pre-existing defects in cardiac function and mitochondrial respiratory capacity in SIRT3(-/-) mice, SIRT3 deficiency does not additionally impair cardiac function following IR or following myocardial infarction.
Find related publications in this database (using NLM MeSH Indexing)
Adenosine Triphosphate - biosynthesis
Animals -
Energy Metabolism -
In Vitro Techniques -
Male -
Mice -
Mice, 129 Strain -
Mice, Knockout -
Mitochondria, Heart - metabolism
Mitochondrial Membrane Transport Proteins - metabolism
Myocardial Contraction -
Myocardial Infarction - physiopathology
Myocardial Reperfusion Injury - genetics
Myocardial Reperfusion Injury - physiopathology
Oxygen Consumption -
RNA, Messenger - genetics
RNA, Messenger - metabolism
Reactive Oxygen Species - metabolism
Sirtuin 3 - deficiency
Sirtuin 3 - genetics
Sirtuin 3 - physiology

Find related publications in this database (Keywords)
mitochondria
sirtuin
heart
ischemia-reperfusion
myocardial infarction
cardiac function
SIRT3
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