Increased muscle PGC-1α expression protects from sarcopenia and metabolic disease during aging

By Tina Wenz, S. Rossi, R. Rotundo, B. Spiegelman, C. Moraes. Proceedings of the National Academy of Sciences of the United States of America, 2009

648 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/efd23d6ad75bbe47adca7970d09e8662190223f0

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

1. M. Sandri
2. Lígia C. Gomes
3. P. Bonaldo
4. B. Spiegelman
5. V. Romanello
6. J. Hawley
7. E. Masiero
8. Jun Wu

In Physiology

1. J. Hawley
2. M. Gibala
3. Jun Wu
4. M. Sandri
5. P. Cohen
6. J. Little
7. Joseph A. Baur
8. D. Sinclair

Citations in the corpus

• FNDC5/Irisin Is Not Only a Myokine but Also an Adipokine (2013, background): “Consequently, mice with transgenically increased PGC1a in their muscles are resistant to age-related obesity and diabetes [11].”
• Adaptive thermogenesis in adipocytes: is beige the new brown? (2013, background): “Muscle-specific ectopic expression of PGC-1a increases whole-body energy expenditure and protects mice from age-related obesity (Wenz et al. 2009).”
• Mitochondrial fission and remodelling contributes to muscle atrophy (2010, background): “Conversely, stimulation of b-oxidative metabolism and mitochondria biogenesis have been shown to reduce muscle wasting in most of these diseases including sarcopenia (Wenz et al, 2009).”
• A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy (2012, neutral): “, 2008) but dramatically protects against the sarcopenia, obesity, and diabetes that accompany aging (Wenz et al., 2009).”
• SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “Interestingly, skeletal muscle-restricted overexpression of PGC-1a is sufficient to delay many agerelated phenotypes and extend mouse life span (Wenz et al., 2009).”
• Cellular and molecular mechanisms of muscle atrophy (2013, background): “…conditions (either in transgenic mice or by transfecting adult myofibers) spares muscle mass during denervation, fasting, heart failure, aging and sarcopenia – similar to the effect observed with expression of constitutively active FoxO3 (Geng et al., 2011; Sandri et al., 2006; Wenz et al., 2009).”
• Physiological adaptations to low‐volume, high‐intensity interval training in health and disease (2012, background): “Given the positive effects that a modest increase in muscle PGC-1α appears to have on oxidative capacity, anti-oxidant defence, glucose uptake, resistance to age-related sarcopenia and anti-inflammatory pathways (Sandri et al. 2006; Benton et al. 2008; Wenz et al. 2009), the increase in PGC-1α follo”
• Mitochondrial DNA: more than an evolutionary bystander (2014, background): “The health benefits of elevated muscle expression of PGC-1a may extend to organismal physiology as transgenic mice with mildly elevated muscle PGC-1a had improved performance in a high-performance exercise test and had a subsequent prolonged life span compared to wild-type animals (Wenz et al. 2009)”