Transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres.

By Jiandie D. Lin, Hai-Ping Wu, Paul T. Tarr, Chen-Yu Zhang, Zhidan Wu, O. Boss, L. F. Michael, P. Puigserver, E. Isotani, E. Olson and 3 more. Nature, 2002

1,321 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7a52036b1b53e5f5fa2f74a7373fd40ea8f62191

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Citations in the corpus

Specific SIRT1 activation mimics low energy levels and protects against diet-induced metabolic disorders by enhancing fat oxidation. (2008, background): “…of skeletal muscle fibers, as the metabolic actions of these transcriptional regulators are stimulated by SIRT1-mediated deacetylation, leading to the promotion of oxidative muscle function (Frescas et al., 2005; Gross et al., 2008; Handschin et al., 2007; Lin et al., 2002; Rodgers et al., 2008).”
Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice (2009, background): “PGC-1α was reported to induce transformation of skeletal muscle fiber from glycolytic type (Type II) into oxidative type (Type I) in transgenic mice (9).”
Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations (2010, unknown): “These results are consistent with reports that mitochondrial biogenesis can drive muscle fiber type switching (Arany et al., 2007; Lin et al., 2002).”
Metabolic Adaptations to Short-term High-Intensity Interval Training: A Little Pain for a Lot of Gain? (2008, background): “This change in phenotype is accompanied by enhanced mitochondrial enzyme expression and an increase in time to fatigue when electrically stimulated (17).”
Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “Transcription factor targets of the PGC-1 coactivators Transcription factor PGC-1α PGC-1β Function References NRF-1 + + mitochondrial genes Wu et al., 1999 NRF-2 + ND mitochondrial genes Mootha et al., 2003 PPARα + + fatty-acid oxidation Vega et al., 2000 PPARβ/δ + ND fatty-acid oxidation Wang et al”
Fiber types in mammalian skeletal muscles. (2011, background): “Transgenic mice overexpressing PGC-1 show increased mitochondrial content and increased levels of oxidative enzymes in fast muscle fibers, as well as an increase in the proportion of type 1 and 2A fibers in fast muscles, thus making the muscles more resistant to fatigue (482, 483, 544).”
Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α (2007, background): “…(2007) 26, 1913–1923 | & 2007 European Molecular Biology Organization |All Rights Reserved 0261-4189/07 www.embojournal.org &2007 European Molecular Biology Organization The EMBO Journal VOL 26 | NO 7 | 2007 EMBO THE JOURNAL 1913 that are rich in mitochondria and highly oxidative (Lin et al, 2002).”
The physiology and pathophysiology of nitric oxide in the brain. (2005, background): “, 2003), and mice overexpressing PGC-1alfa have a larger number of mitochondria in cardiac and skeletal muscles (Lin et al., 2002).”
AMP-Activated Protein Kinase–Deficient Mice Are Resistant to the Metabolic Effects of Resveratrol (2009, background): “Moreover, AMPK can activate PGC-1 , one of Sirt1 substrates, by directly phosphorylating it (50,51), indicating that activation of AMPK can affect the Sirt1dependent pathways in multiple ways.”
Meteorin-like is a hormone that regulates immune-adipose interactions to increase beige fat thermogenesis (2014, background): “Many of the best known benefits of endurance training, such as fiber type switching,mitochondrial biogenesis, and resistance to muscle atrophy, can be stimulated by expression of the transcriptional coactivator PGC1a in the skeletal muscle (Lin et al., 2002).”
Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. (2006, background): “PGC-1a has emerged as a master regulator of mitochondrial biogenesis and respiration (Kelly and Scarpulla, 2004; Lehman et al., 2000; Lin et al., 2002; Puigserver et al., 1998; Wu et al., 1999).”
Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. (2006, background): “Most importantly, PGC-1a controls mitochondrial biogenesis and function, which in the muscle can contribute to fiber-type switching (Lin et al., 2002a) and, in the brown adipose tissue (BAT), to adaptive thermogenesis (Puigserver et al., 1998).”
Resveratrol Ameliorates Aging-Related Metabolic Phenotypes by Inhibiting cAMP Phosphodiesterases (2012, unknown): “It is a coactivator that controls mitochondrial biogenesis and respiration and can contribute to fiber-type switching in skeletal muscle (Lin et al., 2002) and increase adaptive thermogenesis in brown adipose tissue (Puigserver et al.”
Compartment-specific perturbation of protein handling activates genes encoding mitochondrial chaperones (2004, background): “…addressed the role of transcriptional control in cellular adaptation to mitochondrial dysfunction (Liao and Butow, 1993; Amuthan et al., 2001) and have begun to shed light on mechanisms that coordinately upregulate nuclear genes encoding mitochondrial proteins (Wu et al., 1999; Lin et al., 2002).”
Integrative biology of exercise. (2014, unknown): “…limited to, calcium signaling pathways involving calcineurin, calcium-calmodulin-dependent kinase, and the transcriptional cofactors peroxisome proliferator-activated receptor g coactivator 1 a (PGC-1 a ) and PPAR d (Olson and Williams 2000; Lin et al., 2002; Wang et al., 2004; Wu et al., 2002).”
A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine (2005, background): “In the energy utilization tissue, muscle, PGC-1 induces mitochondrial biogenesis through the interaction with NRF1, PPARβ, PPARδ, MEF2, ERR2 (estrogen-related receptor 2), HDAC5, and Gabpa/b (GA-repeat binding protein) (47, 78, 117, 152).”
Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, unknown): “Moreover, PGC-1a enhanced oxidative phosphorylation and appeared a major factor regulating the muscle fiber type favoring the generation of oxidative type 1 muscle fibers (198).”
Regulation of energy metabolism by long-chain fatty acids. (2014, background): “Constitutive expression of PGC1a in skeletal muscle resulted in increased type1 fiber and mitochondrial biogenesis without exercise [169], whereas skeletal muscle specific PGC1a KO mice was unable to adapt to exercise, and became exercise intolerant [170].”