Transcriptional coactivator PGC-1α controls the energy state and contractile function of cardiac muscle
By Zoltan Arany, Huamei He, Jiandie D. Lin, Kirsten Hoyer, Christoph Handschin, O. Toka, Ferhaan Ahmad, T. Matsui, Sherry Chin, Pei-Hsuan Wu and 9 more. 2005
752 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/353a4f9ceb5cd80f272032b3cd907e65e3d8b020
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- R. Scarpulla
- B. Spiegelman
- Christoph Handschin
- Jiandie D. Lin
- D. Kelly
- B. Finck
- Wenli Yang
- Marc Uldry
In Physiology
- R. Scarpulla
- B. Spiegelman
- Christoph Handschin
- Jiandie D. Lin
- D. Kelly
- Wenli Yang
- Marc Uldry
- J. St-Pierre
Citations in the corpus
- Fiber types in mammalian skeletal muscles. (2011, background): “Fast muscles from knockout mice showed an increased level of slow genes, such as slow troponin I and SERCA2; this paradoxical effect was interpreted as the result of the hyperactivity of these animals secondary to alterations in the central nervous system (31).”
- Transcriptional control of mitochondrial biogenesis: the central role of PGC-1alpha. (2008, background): “Two lines of PGC-1a-deficient mice have been independently generated, which differ slightly in their cardiac dysfunction.(21,22) However, somewhat surprisingly, both lines appear to have close to normal mitochondrial volume density in the heart(21,22) yet the expression of mitochondrial genes is blu”
- PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism (2020, background): “Mice genetically deficient in PGC-1α have irregular cardiac energetic reserves [60], respond inefficiently to stressful stimuli, such as transverse aortic banding [211], and present poor contractility responses and heart rates [47].”
- Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “Interestingly, PGC-1α null mice develop early symptoms of heart failure, such as activation of a fetal program of cardiac gene expression and significant increase in circulating levels of atrial natriuretic peptide, a hallmark of cardiac dysfunction (Arany et al., 2005).”
- Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. (2006, background): “In addition, the capacity of the heart to perform basal and strenuous aerobic work is compromised in the mutant mice (Arany et al., 2005; Leone et al., 2005).”
- PGC-1 coactivators: inducible regulators of energy metabolism in health and disease. (2006, background): “Both lines demonstrate that PGC-1α is not essential for the fundamental process of mitochondrial biogenesis in the heart; myocardial mitochondrial volume density is not significantly altered in either Pgc1a–/– line (53, 57).”
- Transcriptional paradigms in mammalian mitochondrial biogenesis and function. (2008, background): “Subsequent experiments with the PGC-1 null mice demonstrated that PGC-1 is not required for mitochondrial biogenesis (9).”