Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Riehle, C; Wende, AR; Zaha, VG; Pires, KM; Wayment, B; Olsen, C; Bugger, H; Buchanan, J; Wang, X; Moreira, AB; Doenst, T; Medina-Gomez, G; Litwin, SE; Lelliott, CJ; Vidal-Puig, A; Abel, ED.
PGC-1β deficiency accelerates the transition to heart failure in pressure overload hypertrophy.
Circ Res. 2011; 109(7): 783-793.
Doi: 10.1161/CIRCRESAHA.111.243964
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- Co-Autor*innen der Med Uni Graz
- Bugger Heiko Matthias
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- Abstract:
- Pressure overload cardiac hypertrophy, a risk factor for heart failure, is associated with reduced mitochondrial fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) proteins that correlate in rodents with reduced PGC-1α expression. To determine the role of PGC-1β in maintaining mitochondrial energy metabolism and contractile function in pressure overload hypertrophy. PGC-1β deficient (KO) mice and wildtype (WT) controls were subjected to transverse aortic constriction (TAC). Although LV function was modestly reduced in young KO hearts, there was no further decline with age so that LV function was similar between KO and WT when TAC was performed. WT-TAC mice developed relatively compensated LVH, despite reduced mitochondrial function and repression of OXPHOS and FAO genes. In nonstressed KO hearts, OXPHOS gene expression and palmitoyl-carnitine-supported mitochondrial function were reduced to the same extent as banded WT, but FAO gene expression was normal. Following TAC, KO mice progressed more rapidly to heart failure and developed more severe mitochondrial dysfunction, despite a similar overall pattern of repression of OXPHOS and FAO genes as WT-TAC. However, in relation to WT-TAC, PGC-1β deficient mice exhibited greater degrees of oxidative stress, decreased cardiac efficiency, lower rates of glucose metabolism, and repression of hexokinase II protein. PGC-1β plays an important role in maintaining baseline mitochondrial function and cardiac contractile function following pressure overload hypertrophy by preserving glucose metabolism and preventing oxidative stress.
- Find related publications in this database (using NLM MeSH Indexing)
- Aging -
- Animals -
- Blood Pressure -
- Disease Models, Animal -
- Disease Progression -
- Energy Metabolism - genetics
- Fatty Acids - metabolism
- Gene Expression Regulation -
- Glucose - metabolism
- Heart Failure - diagnostic imaging
- Heart Failure - etiology
- Heart Failure - genetics
- Heart Failure - metabolism
- Heart Failure - physiopathology
- Heart Failure - prevention & control
- Hexokinase - metabolism
- Hypertrophy, Left Ventricular - complications
- Hypertrophy, Left Ventricular - diagnostic imaging
- Hypertrophy, Left Ventricular - physiopathology
- Mice -
- Mice, Knockout -
- Mitochondria, Heart - metabolism
- Myocardial Contraction -
- Myocardium - metabolism
- Oxidation-Reduction -
- Oxidative Phosphorylation -
- Oxidative Stress -
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha -
- Trans-Activators - deficiency
- Trans-Activators - genetics
- Transcription Factors -
- Ultrasonography -
- Ventricular Dysfunction, Left - diagnostic imaging
- Ventricular Dysfunction, Left - etiology
- Ventricular Dysfunction, Left - genetics
- Ventricular Dysfunction, Left - metabolism
- Ventricular Dysfunction, Left - physiopathology
- Ventricular Dysfunction, Left - prevention & control
- Ventricular Function, Left -
- Find related publications in this database (Keywords)
- mitochondria
- cardiac hypertrophy
- heart failure
- gene expression