Increased Adenine Nucleotide Degradation in Skeletal Muscle Atrophy

Miller, Spencer G.; Hafen, Paul S.; Brault, Jeffrey J.

doi:10.3390/ijms21010088

Cited by 49 publications

(29 citation statements)

References 152 publications

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“…It is known that mitochondria are crucial for providing energy to muscle contraction, and dramatic reduction in total adenine nucleotides (ATP, ADP, and AMP) is observed in atrophic skeletal muscle ( 39 ). Normal mitochondrial membrane potential is prerequisite of the normal functions such as oxidative phosphorylation and ATP generation ( 27 ), and our study found that apigenin can help to maintain the membrane potential.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant Apigenin Relieves Age-Related Muscle Atrophy by Inhibiting Oxidative Stress and Hyperactive Mitophagy and Apoptosis in Skeletal Muscle of Mice

Wang

Yang

Zou

et al. 2020

The Journals of Gerontology: Series A

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Skeletal muscle atrophy in the elderly causes loss in muscle mass and functions. Naturally-occurring antioxidant flavonoid apigenin is able to ameliorate obesity-and denervation-induced muscle atrophies, but its effects on age-related muscle atrophy remains unknown. We hypothesized that apigenin can relieve muscle atrophy in aged mice, probably through special effects on reactive oxygen species and enzymes with antioxidant functions. For the male mice of the study, apigenin showed significant dose-dependent effects in relieving aging-related muscle atrophy according to results of frailty index as indicator of frailty associated with ageing, grip strength and running distance. Apigenin also improved myofiber size and morphological features and increased mitochondria number and volume, as manifested by succinate dehydrogenase staining and transmission electron microscopy. Our tests also suggested that apigenin promoted activities of enzymes such as superoxide dismutase and glutathione peroxidase for antioxidation and those for aerobic respiration such as mitochondrial respiratory enzyme complexes I, II and IV, increased ATP, and enhanced expression of genes such as peroxisome proliferator-activated receptor-γ coactivator 1α, mitochondrial transcription factor A, nuclear respiratory factor-1, and ATP5B involved in mitochondrial biogenesis. The data also suggested that apigenin inhibited Bcl-2/adenovirus E1B 19kD-interacting protein 3 and DNA fragmentation as indicators of mitophagy and apoptosis in aged mice with skeletal muscle atrophy. Together, the results suggest that apigenin relieves age-related skeletal muscle atrophy through reducing oxidative stress and inhibiting hyperactive autophagy and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Antioxidant Apigenin Relieves Age-Related Muscle Atrophy by Inhibiting Oxidative Stress and Hyperactive Mitophagy and Apoptosis in Skeletal Muscle of Mice

Wang

Yang

Zou

et al. 2020

The Journals of Gerontology: Series A

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“…In addition, the data in Figures S5,S6 reveal that Xid mice restored metabolites 7 times more than ibrutinib-treated mice ( Figure S7 ). Many of the additionally restored metabolites in Xid mice are known to be deregulated in sepsis such as adenine ( 73 ) creatinine ( 74 ), and kynurenine ( 75 ). An explanation for the different magnitude of restored metabolites in Xid mice in comparison with ibrutinib-treated mice could be the different number of inhibited kinases.…”

Section: Discussionmentioning

confidence: 99%

X-Linked Immunodeficient Mice With No Functional Bruton's Tyrosine Kinase Are Protected From Sepsis-Induced Multiple Organ Failure

et al. 2020

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We previously reported the Bruton's tyrosine kinase (BTK) inhibitors ibrutinib and acalabrutinib improve outcomes in a mouse model of polymicrobial sepsis. Now we show that genetic deficiency of the BTK gene alone in Xid mice confers protection against cardiac, renal, and liver injury in polymicrobial sepsis and reduces hyperimmune stimulation (“cytokine storm”) induced by an overwhelming bacterial infection. Protection is due in part to enhanced bacterial phagocytosis in vivo , changes in lipid metabolism and decreased activation of NF-κB and the NLRP3 inflammasome. The inactivation of BTK leads to reduced innate immune cell recruitment and a phenotypic switch from M1 to M2 macrophages, aiding in the resolution of sepsis. We have also found that BTK expression in humans is increased in the blood of septic non-survivors, while lower expression is associated with survival from sepsis. Importantly no further reduction in organ damage, cytokine production, or changes in plasma metabolites is seen in Xid mice treated with the BTK inhibitor ibrutinib, demonstrating that the protective effects of BTK inhibitors in polymicrobial sepsis are mediated solely by inhibition of BTK and not by off-target effects of this class of drugs.

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“…It regulates blood flow to skeletal muscle [ 73 ], and synergistically affects insulin-stimulated glucose uptake and contraction in skeletal muscle [ 74 ]. Most of the physiological effects of adenosine are regulated via specific adenosine receptors [ 75 ], such as A1R, a cytoprotective of skeletal muscle [ 76 ]. TRPV4, a member of TRP channel superfamily plays a mechanosensory or osmosensory function in many musculoskeletal tissues and inhibits bone loss or muscular atrophy [ 77 ].…”

Section: Discussionmentioning

confidence: 99%

Tart Cherry (Fruit of Prunus cerasus) Concentrated Powder (TCcp) Ameliorates Glucocorticoid-Induced Muscular Atrophy in Mice

Lim²,

Cho³

et al. 2021

Medicina

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Background and Objectives: The present study investigated the beneficial effects of tart cherry (fruit of Prunus cerasus) concentrated powder (TCcp) on glucocorticoid (GLU)-induced catabolic muscular atrophy in the skeletal muscle of mice. Furthermore, its potential mechanism was also studied. Materials and Methods: Changes in calf thickness, calf muscle weight, calf muscle strength, body weight, gastrocnemius muscle histology, immunohistochemistry, serum creatinine, creatine kinase, lactate dehydrogenase, and antioxidant defense systems were measured. Malondialdehyde, reactive oxygen species, glutathione content, catalase, and superoxide dismutase activities in the gastrocnemius muscle, and muscle-specific mRNA expressions were evaluated. Results: After 24 days, GLU control mice showed muscular atrophy at all criteria of indexes. The muscular atrophy symptoms were significantly inhibited by oral treatment with 250 mg/kg and 500 mg/kg of TCcp through antioxidative and anti-inflammatory modulated expression of genes involved in muscle protein degradation (myostatin, atrogin-1, SIRT1, and MuRF1) and synthesis (A1R, Akt1, TRPV4, and PI3K). Conclusions: This study shows that the TCcp (500 mg/kg and 250 mg/kg) could improve muscular atrophies caused by various etiologies.

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Increased Adenine Nucleotide Degradation in Skeletal Muscle Atrophy

Cited by 49 publications

References 152 publications

Antioxidant Apigenin Relieves Age-Related Muscle Atrophy by Inhibiting Oxidative Stress and Hyperactive Mitophagy and Apoptosis in Skeletal Muscle of Mice

Antioxidant Apigenin Relieves Age-Related Muscle Atrophy by Inhibiting Oxidative Stress and Hyperactive Mitophagy and Apoptosis in Skeletal Muscle of Mice

X-Linked Immunodeficient Mice With No Functional Bruton's Tyrosine Kinase Are Protected From Sepsis-Induced Multiple Organ Failure

Tart Cherry (Fruit of Prunus cerasus) Concentrated Powder (TCcp) Ameliorates Glucocorticoid-Induced Muscular Atrophy in Mice

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