Adaptations of skeletal muscle to exercise: rapid increase in the transcriptional coactivator PGC‐1

By K. Baar, Adam R. Wende, T. Jones, Matthew Marison, L. Nolte, May M. Chen, D. Kelly, J. Holloszy. The FASEB Journal, 2002

1,090 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/5ad501bf41f25fed10b1e5b3c3fa99c0938d1739

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Citations in the corpus

PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism (2020, background): “Another experiment established the relationship between mitochondrial biogenesis and exercise by an acute swimming bout, which increased PGC-1α protein expression and NRF2 binding to the cyclooxygenase (COX) IV promoter and NRF-1 binding to the δ-ALAS (δ-aminolevulinate synthase) promoter [69].”
Transcriptional control of mitochondrial biogenesis and function. (2009, background): “Single bouts of exercise lead to transient increases in the levels of PGC-1α, PRC, NRF-1, GABP, ERRα, PPARδ, and downstream mitochondrial targets (22, 24, 25, 127, 131).”
Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “In fact, both PGC-1α and β mRNAs are alternatively spliced to generate multiple isoforms, though the functional significance of this remains unknown (Baar et al., 2002; Kamei et al., 2003; Meirhaeghe et al., 2003).”
Transcriptional regulatory circuits controlling mitochondrial biogenesis and function. (2004, background): “It was subsequently shown that PGC-1 gene expression is induced by exercise in rodent and human skeletal muscle (Goto et al. 2000; Baar et al. 2002; Terada et al. 2002; Terada and Tabata 2003; Pilegaard et al. 2003) and by short-term starvation in the heart and liver of mice (Lehman et al.”
AMPK in Health and Disease. (2009, background): “Since the constitutively active AMPK fragment 1 (1-312) is not activated by the PT1 compound, it is proposed that PT1 acts by reversing the autoinhibition of the AIS (313-335).”
Regulation of mitochondrial biogenesis (2010, neutral): “COX IV promoter [12].”
Fiber types in mammalian skeletal muscles. (2011, background): “PGC-1 is expressed at higher levels in slow than fast muscles and is readily induced by exercise in both rodents and humans (37, 674, 786, 886).”
Exercise metabolism and the molecular regulation of skeletal muscle adaptation. (2013, background): “Even when total training time and energy expenditure have been reduced by 80% and 90%, respectively, improvements of VO2max, muscle oxidative capacity, and insulin sensitivity are comparable to traditional aerobic training (Burgomaster et al., 2008; Babraj et al., 2009).”
PGC-1 coactivators: inducible regulators of energy metabolism in health and disease. (2006, background): “Studies in rodent models indicate that both short-term exercise and endurance training activate PGC-1α expression in skeletal muscle (34, 35, 64, 65).”
Cancer cachexia: mediators, signaling, and metabolic pathways. (2012, background): “PGC-1a is highly induced during exercise, and one of the primary roles of this factor is to regulate mitochondrial biogenesis and oxidative phosphorylation in myofibers, characteristic of type I, fatigue-resistant, muscles (Lin et al., 2002; Baar et al., 2002).”
The Molecular Bases of Training Adaptation (2007, background): “Endurance exercise has been routinely shown as a potent stimulator of PGC-1α gene and protein expression (Pilegaard et al. 2000; Baar et al. 2002; Norrbom et al. 2003; Psilander et al. 2003; Terada and Tabata 2003; Cluberton et al. 2005; Jorgensen et al. 2005; Terada et al. 2005).”