Interactions between ROS and AMP kinase activity in the regulation of PGC-1α transcription in skeletal muscle cells

Irrcher, Isabella; Ljubicic, Vladimir; Hood, David A.

doi:10.1152/ajpcell.00267.2007

Cited by 324 publications

(298 citation statements)

References 44 publications

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“…The involvement of ROS in the expression of PGC-1α was first demonstrated in myotube cultures, where the up-regulation of PGC-1α mRNA following acute and chronic electrical stimulation, or hydrogen peroxide incubation was attenuated in the presence of antioxidants or ROS scavengers, respectively (Irrcher et al, 2009;Silveira et al, 2006). Intriguingly, ROS has shown to induce/activate PGC-1α via multiple signalling pathways involving AMPK, p38 MAPK and nitric oxide signalling.…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

“…Intriguingly, ROS has shown to induce/activate PGC-1α via multiple signalling pathways involving AMPK, p38 MAPK and nitric oxide signalling. For instance, ROS may initiate PGC-1α transcription and activity via AMPK, as C2C12 myotubes incubated with hydrogen peroxide increased AMPK phosphorylation and subsequently PGC-1α activity and mRNA expression (Irrcher et al, 2009). Further, p38 MAPK activation and endothelial nitric oxide synthase expression, both upstream targets of PGC-1α, has shown to be attenuated in exercising rats administered with allopurinol (Gomez-Cabrera et al, 2005).…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

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PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Ihsan¹,

Watson²,

Abbiss³

2014

Cell Mol Exerc Physiol

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PGC-1α is regarded as a key regulator of mitochondrial biogenesis due to its central role in regulating the activity of key transcription factors associated with encoding mitochondrial components. Additionally, PGC-1α has shown to mediate adaptations that increase fat metabolism and angiogenesis, contributing to the overall oxidative phenotype of the muscle. While it is well established that exercise is a potent stimulator of PGC-1α, recent evidence indicates that heat and cold exposures may also influence mitochondrial biogenesis through the up-regulation of PGC-1α. This highlights the potential use of these modalities in conjunction with exercise to enhance training adaptations. As such, the purpose of this review is to describe the possible mechanisms and pathways by which exercise, as well as hot and cold exposures may influence mitochondrial biogenesis. It is clear that changes in intracellular calcium, oxidative stress and phosphorylation potential are major up-regulators of PGC-1α during exercise. Moreover, there is evidence implicating calcium signalling, in addition to β-adrenergic activation in cold-induced mitochondrial biogenesis, while PGC-1α during heat exposure is likely triggered by changes in phosphorylation potential and nitric oxide signalling. However, these mechanisms appear to change considerably when cold/heat is administered following exercise, and seem to be dependent on the experimental models used (i.e. in vitro vs. in vivo, rodent vs. human). Understanding the effects heat/cold exposure and its interaction with exercise may lead to the optimisation and development of temperature-related interventions to enhance training adaptations, or aid in the treatment of mitochondrial related diseases.

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Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Ihsan¹,

Watson²,

Abbiss³

2014

Cell Mol Exerc Physiol

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“…Activated CaMK Ⅱ further phosphorylates its downstream kinase p38 mitogen-activated protein kinase (MAPK), which results in the rapid activation of preexisting PGC-1α proteins, followed by increases in PGC-1α protein expression 34,35) . The basal level of ROS stabilizes PGC-1α mRNA, contributing to the maintenance of PGC-1α expression 36) . On the other hand, an elevated level of ROS activates AMPK, thus leading to an increase in PGC-1α promoter activity and mRNA level 36) .…”

Section: Intracellular Signaling Involved In Endurance Traininginducementioning

confidence: 99%

“…The basal level of ROS stabilizes PGC-1α mRNA, contributing to the maintenance of PGC-1α expression 36) . On the other hand, an elevated level of ROS activates AMPK, thus leading to an increase in PGC-1α promoter activity and mRNA level 36) . ROS are also suggested to regulate PGC-1α expression via the p38 MAPK and NFκB pathways 37) .…”

Section: Intracellular Signaling Involved In Endurance Traininginducementioning

confidence: 99%

Reactive oxygen species and endurance training-induced adaptations

Matsui

2013

JPFSM

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Endurance training induces mitochondrial biogenesis and angiogenesis in skeletal muscle. Endurance training also improves insulin sensitivity at both the skeletal muscle and whole body level. Recently, ROS have been suggested to play an important role in endurance training-induced adaptations. However, this hypothesis is not yet fully supported. To advance understanding of the role of ROS and antioxidants in endurance training-induced adaptations, efforts should be made in future studies to clarify the sites of ROS production and the influence of antioxidants on the redox status under each training condition. Effort should also be directed to identifying the signaling pathways involved. In this situation, it should be recognized that in vivo cellular signaling is redundant. Therefore, efforts to evaluate the relative importance and interactions among the multiple cellular signaling pathways involved in each training condition are required. Without elucidating the role of ROS and antioxidants in endurance traininginduced adaptations, then evidence-based sound advice regarding antioxidant supplementation cannot be made.

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“…Endurance exercise increases mitochondrial activity and content, while insulin resistance is associated with defects in mitochondrial lipid catabolism and accumulation of ectopic lipids. AMPK was found to directly phosphorylate and thus activate PGC-1a (Jager et al 2007), which has a crucial role in enhancing mitochondrial biogenesis in SM and BAT, and up-regulate expression of the PGC-1a gene (Irrcher et al 2009), in association with a shift of SM fibers toward a more oxidative phenotype (McGee and Hargreaves 2010). Involvement of AMPK in the stimulation of lipid catabolism in SM by leptin ) is discussed below (see ''Treatments enhancing energy expenditure'' section).…”

Section: Ampk Function In Smmentioning

confidence: 99%

Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase

et al. 2011

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Strategies to prevent and treat obesity aim to decrease energy intake and/or increase energy expenditure. Regarding the increase of energy expenditure, two key intracellular targets may be considered (1) mitochondrial oxidative phosphorylation, the major site of ATP production, and (2) AMP-activated protein kinase (AMPK), the master regulator of cellular energy homeostasis. Experiments performed mainly in transgenic mice revealed a possibility to ameliorate obesity and associated disorders by mitochondrial uncoupling in metabolically relevant tissues, especially in white adipose tissue (WAT), skeletal muscle (SM), and liver. Thus, ectopic expression of brown fat-specific mitochondrial uncoupling protein 1 (UCP1) elicited major metabolic effects both at the cellular/tissue level and at the whole-body level. In addition to expected increases in energy expenditure, surprisingly complex phenotypic effects were detected. The consequences of mitochondrial uncoupling in WAT and SM are not identical, showing robust and stable obesity resistance accompanied by improvement of lipid metabolism in the case of ectopic UCP1 in WAT, while preservation of insulin sensitivity in the context of high-fat feeding represents the major outcome of muscle UCP1 expression. These complex responses could be largely explained by tissue-specific activation of AMPK, triggered by a depression of cellular energy charge. Experimental data support the idea that (1) while being always activated in response to mitochondrial uncoupling and compromised intracellular energy status in general, AMPK could augment energy expenditure and mediate local as well as whole-body effects; and (2) activation of AMPK alone does not lead to induction of energy expenditure and weight reduction.

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Interactions between ROS and AMP kinase activity in the regulation of PGC-1α transcription in skeletal muscle cells

Cited by 324 publications

References 44 publications

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Reactive oxygen species and endurance training-induced adaptations

Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase

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