Skeletal muscle mitochondria: A major player in exercise, health and disease

Russell, Aaron P.; Foletta, Victoria C.; Snow, Rod J.; Wadley, Glenn D.

doi:10.1016/j.bbagen.2013.11.016

Cited by 199 publications

(170 citation statements)

References 138 publications

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“…Dysfunctional mitochondria are recognized as a major factor contributing to the age-related loss of muscle mass, sarcopenia. 58,79,80 Both Pompe and aging muscle exhibit inadequate Ca 2C control and apoptosis of some of the nuclei in multinucleated muscle cells (syncytial apoptosis); the latter can cause myofiber atrophy without myofiber death. 81 Our current findings of decreased oxygen consumption, increased oxidative stress, and activation of apoptosis in Pompe muscle cells, as well as our previous data on autophagic block (a failure of autophagosomal-lysosomal fusion) and the buildup of lipofuscin in muscle tissue of both KO mice and Pompe patients, 29,30 all support the similarity between Pompe and aged muscle.…”

Section: Discussionmentioning

confidence: 99%

Defects in calcium homeostasis and mitochondria can be reversed in Pompe disease

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Defects in calcium homeostasis and mitochondria can be reversed in Pompe disease

et al. 2015

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“…137 The CREB, in turn is regulated by PPARα, another transcription factor, known for regulating fatty acid catabolism in the liver and upregulated in muscle by exercise 138,139 but expressed also in hippocampal neurons. 140 The PGC-1α, an important mediator of exercise-induced mitochondrial proliferation in skeletal muscle, 141 is expressed also in neurons in the hippocampus, where it mediates exercise-induced elevation of BDNF through enhancing the expression of a membrane protein known as fibronectin type III domain-containing protein 5 and its cleavage product irisin, a 112 amino-acid peptide myokine. 142 The cAMP-reducing effect of HCAR1 would be expected to reduce the CREB-dependent influence on memory and BDNF, but a noncanonical effect of HCAR1 would have the opposite effect on BDNF (see above) and might even regulate PPARα, PGC-1α, and irisin.…”

Section: Targets For New Therapeutic Drugs and Interventions Neuropromentioning

confidence: 99%

Lactate Transport and Signaling in the Brain: Potential Therapeutic Targets and Roles in Body—Brain Interaction

Bergersen

2014

J Cereb Blood Flow Metab

199

166

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Lactate acts as a 'buffer' between glycolysis and oxidative metabolism. In addition to being exchanged as a fuel by the monocarboxylate transporters (MCTs) between cells and tissues with different glycolytic and oxidative rates, lactate may be a 'volume transmitter' of brain signals. According to some, lactate is a preferred fuel for brain metabolism. Immediately after brain activation, the rate of glycolysis exceeds oxidation, leading to net production of lactate. At physical rest, there is a net efflux of lactate from the brain into the blood stream. But when blood lactate levels rise, such as in physical exercise, there is net influx of lactate from blood to brain, where the lactate is used for energy production and myelin formation. Lactate binds to the lactate receptor GPR81 aka hydroxycarboxylic acid receptor (HCAR1) on brain cells and cerebral blood vessels, and regulates the levels of cAMP. The localization and function of HCAR1 and the three MCTs (MCT1, MCT2, and MCT4) expressed in brain constitute the focus of this review. They are possible targets for new therapeutic drugs and interventions. The author proposes that lactate actions in the brain through MCTs and the lactate receptor underlie part of the favorable effects on the brain resulting from physical exercise.

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“…The peroxisome-proliferator-activated receptor γ coactivator 1α (PGC1-α; also known as PPARGC1A) is one of the key regulators of the oxidative metabolism of muscle, increasing mitochondrial biogenesis and augmenting the expression of enzymes in the electron transport system, such as cytochrome c oxidase (COX) and succinate dehydrogenase (SDH) (Garcia-Roves et al, 2006;Russell et al, 2014). Real-time PCR analysis revealed that PGC1-α expression was significantly decreased in skeletal muscle cells (C2C12) that had been infected with an adenovirus construct expressing a small hairpin (sh)RNA against NRIP (named Ad-shNRIP) to knockdown endogenous NRIP expression (Fig.…”

Section: Nrip Has An Effect On Mitochondrial Activitymentioning

confidence: 99%

NRIP is a novel Z-disc protein to activate calmodulin signaling for skeletal muscle contraction and regeneration

Chen

Yan

et al. 2015

Journal of Cell Science

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Nuclear receptor interaction protein (NRIP, also known as DCAF6 and IQWD1) is a Ca 2+ -dependent calmodulin-binding protein.In this study, we newly identify NRIP as a Z-disc protein in skeletal muscle. NRIP-knockout mice were generated and found to have reduced muscle strength, susceptibility to fatigue and impaired adaptive exercise performance. The mechanisms of NRIP-regulated muscle contraction depend on NRIP being downstream of Ca 2+ signaling, where it stimulates activation of both 'calcineurin-nuclear factor of activated T-cells, cytoplasmic 1' (CaN-NFATc1; also known as NFATC1) and calmodulin-dependent protein kinase II (CaMKII) through interaction with calmodulin (CaM), resulting in the induction of mitochondrial activity and the expression of genes encoding the slow class of myosin, and in the regulation of Ca 2+ homeostasis through the internal Ca 2+ stores of the sarcoplasmic reticulum. Moreover, NRIP-knockout mice have a delayed regenerative capacity. The amount of NRIP can be enhanced after muscle injury and is responsible for muscle regeneration, which is associated with the increased expression of myogenin, desmin and embryonic myosin heavy chain during myogenesis, as well as for myotube formation. In conclusion, NRIP is a novel Z-disc protein that is important for skeletal muscle strength and regenerative capacity.

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Skeletal muscle mitochondria: A major player in exercise, health and disease

Cited by 199 publications

References 138 publications

Defects in calcium homeostasis and mitochondria can be reversed in Pompe disease

Defects in calcium homeostasis and mitochondria can be reversed in Pompe disease

Lactate Transport and Signaling in the Brain: Potential Therapeutic Targets and Roles in Body—Brain Interaction

NRIP is a novel Z-disc protein to activate calmodulin signaling for skeletal muscle contraction and regeneration

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