scholarly journals Ischaemic exercise enhances mitochondrial and ion transport gene adaptations in trained human skeletal muscle: Role of cellular redox state, AMPK and CaMKII signalling

2017 ◽  
Vol 66 (1) ◽  
pp. 75-75
Author(s):  
Danny Christiansen ◽  
Robyn M. Murphy ◽  
D. J. Bishop
Keyword(s):  
Skeletal Muscle ◽  
Ion Transport ◽  
Human Skeletal Muscle ◽  
Redox State ◽  
Cellular Redox ◽  
Cellular Redox State

scholarly journals Toxicity and Antigenotoxic Effect of Hispolon Derivatives: Role of Structure in Modulating Cellular Redox State and Thioredoxin Reductase

ACS Omega ◽  
2018 ◽  
Vol 3 (6) ◽  
pp. 5958-5970 ◽  
Author(s):  
Pogakula Chethna ◽  
Shruti S. Iyer ◽  
Vishwa V. Gandhi ◽  
Amit Kunwar ◽  
Beena G. Singh ◽  
...  
Keyword(s):  
Redox State ◽  
Thioredoxin Reductase ◽  
Cellular Redox ◽  
Antigenotoxic Effect ◽  
Cellular Redox State

The role of agrin during the maturation of human skeletal muscle fibres

2006 ◽  
Vol 99 (2-3) ◽  
pp. 1
Author(s):  
Fabio Ruzzier ◽  
Elena Bandi ◽  
Mihaela Jurdana ◽  
Paola Lorenzon ◽  
Marina Sciancalepore
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Muscle Fibres ◽  
Skeletal Muscle Fibres

scholarly journals Cellular Redox State Acts as Switch to Determine the Direction of NNT-Catalyzed Reaction in Cystic Fibrosis Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 967
Author(s):  
Maria Favia ◽  
Anna Atlante
Keyword(s):  
Cystic Fibrosis ◽  
Redox State ◽  
Molecular Mechanisms ◽  
Activity Level ◽  
Cellular Redox ◽  
Redox States ◽  
Mitochondrial Ros ◽  
New Information ◽  
Cellular Dysfunction ◽  
Cellular Redox State

The redox states of NAD and NADP are linked to each other in the mitochondria thanks to the enzyme nicotinamide nucleotide transhydrogenase (NNT) which, by utilizing the mitochondrial membrane potential (mΔΨ), catalyzes the transfer of redox potential between these two coenzymes, reducing one at the expense of the oxidation of the other. In order to define NNT reaction direction in CF cells, NNT activity under different redox states of cell has been investigated. Using spectrophotometric and western blotting techniques, the presence, abundance and activity level of NNT were determined. In parallel, the levels of NADPH and NADH as well as of mitochondrial and cellular ROS were also quantified. CF cells showed a 70% increase in protein expression compared to the Wt sample; however, regarding NNT activity, it was surprisingly lower in CF cells than healthy cells (about 30%). The cellular redox state, together with the low mΔΨ, pushes to drive NNT reverse reaction, at the expense of its antioxidant potential, thus consuming NADPH to support NADH production. At the same time, the reduced NNT activity prevents the NADH, produced by the reaction, from causing an explosion of ROS by the damaged respiratory chain, in accordance with the reduced level of mitochondrial ROS in NNT-loss cells. This new information on cellular bioenergetics represents an important building block for further understanding the molecular mechanisms responsible for cellular dysfunction in cystic fibrosis.

A Novel Redox Based Therapy Targets the Malignant Cellular Redox State

2016 ◽  
Vol 100 ◽  
pp. S119 ◽  
Author(s):  
Dustin Carroll ◽  
Yanming Zhao ◽  
Haining Zhu ◽  
Ines Batinic-Haberle ◽  
Daret St. Clair
Keyword(s):  
Redox State ◽  
Cellular Redox ◽  
Therapy Targets ◽  
Cellular Redox State

scholarly journals FGF-2–dependent signaling activated in aged human skeletal muscle promotes intramuscular adipogenesis

2021 ◽  
Vol 118 (37) ◽  
pp. e2021013118 ◽  
Author(s):  
Sebastian Mathes ◽  
Alexandra Fahrner ◽  
Umesh Ghoshdastider ◽  
Hannes A. Rüdiger ◽  
Michael Leunig ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transcriptional Activation ◽  
Human Skeletal Muscle ◽  
Muscle Growth ◽  
Muscle Cells ◽  
Adeno Associated Virus ◽  
Adult Skeletal Muscle

Aged skeletal muscle is markedly affected by fatty muscle infiltration, and strategies to reduce the occurrence of intramuscular adipocytes are urgently needed. Here, we show that fibroblast growth factor-2 (FGF-2) not only stimulates muscle growth but also promotes intramuscular adipogenesis. Using multiple screening assays upstream and downstream of microRNA (miR)-29a signaling, we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle of aged mice and humans. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1, which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and adeno-associated virus–mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular adipose tissue (IMAT) formation in vivo. Skeletal muscle from human donors aged >75 y versus <55 y showed activation of FGF-2–dependent signaling and increased IMAT. Thus, our data highlights a disparate role of FGF-2 in adult skeletal muscle and reveals a pathway to combat fat accumulation in aged human skeletal muscle.

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