PGC-1α-mediated regulation of mitochondrial function and physiological implications
Publikation: Bidrag til tidsskrift › Review › fagfællebedømt
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PGC-1α-mediated regulation of mitochondrial function and physiological implications. / Halling, Jens Frey; Pilegaard, Henriette.
I: Applied Physiology, Nutrition and Metabolism, Bind 45, Nr. 9, 2020, s. 927-936.Publikation: Bidrag til tidsskrift › Review › fagfællebedømt
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TY - JOUR
T1 - PGC-1α-mediated regulation of mitochondrial function and physiological implications
AU - Halling, Jens Frey
AU - Pilegaard, Henriette
N1 - (Ekstern)
PY - 2020
Y1 - 2020
N2 - The majority of human energy metabolism occurs in skeletal muscle mitochondria emphasizing the importance of understanding the regulation of myocellular mitochondrial function. The transcriptional co-activator PGC-1α has been characterized as a major factor in the transcriptional control of several mitochondrial components. Thus, PGC-1α is often described as a master regulator of mitochondrial biogenesis as well as a central player in regulating the anti-oxidant defense. However, accumulating evidence suggests that PGC-1α is also involved in the complex regulation of mitochondrial quality beyond biogenesis, which includes mitochondrial network dynamics and autophagic removal of damaged mitochondria. In addition, mitochondrial ROS production has been suggested to regulate skeletal muscle insulin sensitivity, which may also be influenced by PGC-1α. This review aims to highlight the current evidence for PGC-1α-mediated regulation of skeletal muscle mitochondrial function beyond the effects on mitochondrial biogenesis as well as the potential PGC-1α-related impact on insulin-stimulated glucose uptake in skeletal muscle. Novelty: • PGC-1α regulates mitochondrial biogenesis, but also has effects on mitochondrial functions beyond biogenesis. • Mitochondrial quality control mechanisms, including fission, fusion and mitophagy, are regulated by PGC-1α. • PGC-1α-mediated regulation of mitochondrial quality may affect age-related mitochondrial dysfunction and insulin sensitivity.
AB - The majority of human energy metabolism occurs in skeletal muscle mitochondria emphasizing the importance of understanding the regulation of myocellular mitochondrial function. The transcriptional co-activator PGC-1α has been characterized as a major factor in the transcriptional control of several mitochondrial components. Thus, PGC-1α is often described as a master regulator of mitochondrial biogenesis as well as a central player in regulating the anti-oxidant defense. However, accumulating evidence suggests that PGC-1α is also involved in the complex regulation of mitochondrial quality beyond biogenesis, which includes mitochondrial network dynamics and autophagic removal of damaged mitochondria. In addition, mitochondrial ROS production has been suggested to regulate skeletal muscle insulin sensitivity, which may also be influenced by PGC-1α. This review aims to highlight the current evidence for PGC-1α-mediated regulation of skeletal muscle mitochondrial function beyond the effects on mitochondrial biogenesis as well as the potential PGC-1α-related impact on insulin-stimulated glucose uptake in skeletal muscle. Novelty: • PGC-1α regulates mitochondrial biogenesis, but also has effects on mitochondrial functions beyond biogenesis. • Mitochondrial quality control mechanisms, including fission, fusion and mitophagy, are regulated by PGC-1α. • PGC-1α-mediated regulation of mitochondrial quality may affect age-related mitochondrial dysfunction and insulin sensitivity.
U2 - 10.1139/apnm-2020-0005
DO - 10.1139/apnm-2020-0005
M3 - Review
C2 - 32516539
VL - 45
SP - 927
EP - 936
JO - Applied Physiology, Nutrition and Metabolism
JF - Applied Physiology, Nutrition and Metabolism
SN - 1715-5312
IS - 9
ER -
ID: 242712800