Reactive oxygen species and calcium signals in skeletal muscle: A crosstalk involved in both normal signaling and disease
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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Reactive oxygen species and calcium signals in skeletal muscle: A crosstalk involved in both normal signaling and disease. / Espinosa, Alejandra; Henríquez-Olguín, Carlos; Jaimovich, Enrique.
I: Cell Calcium, Bind 60, Nr. 3, 2016, s. 172-179.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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TY - JOUR
T1 - Reactive oxygen species and calcium signals in skeletal muscle: A crosstalk involved in both normal signaling and disease
AU - Espinosa, Alejandra
AU - Henríquez-Olguín, Carlos
AU - Jaimovich, Enrique
N1 - Publisher Copyright: © 2016 Elsevier Ltd
PY - 2016
Y1 - 2016
N2 - Reactive Oxygen Species (ROS) have been profusely studied as agents of potential damage to living cells and they have been related to a number of pathological processes. Increasing evidence points to a more positive role of ROS in cell signaling and the detailed mechanism that regulates the precise amount of ROS needed for cell functioning without the deleterious effects of excess ROS still needs to be resolved in detail. In skeletal muscle the main source of ROS during normal functioning appears to be NADPH oxidase 2 (NOX2), which is activated by electrical stimuli (or exercise) through a cascade of events that include ATP release through pannexin1 channels. NOX2 is a protein complex that assembles in the T-tubule membrane before activation and ROS production by NOX2 appears to be important for muscle adaptation through gene expression and mitochondrial biogenesis as well as for improving glucose transport after insulin action. Excess ROS production (or diminished antioxidant defenses) plays a role in a number of pathological processes in skeletal muscle. Together with increased reactive nitrogen species, an increase in ROS appears to have a deleterious role in a model of Duchenne muscular dystrophy as well as muscle wasting in other diseases such as aging sarcopenia and cancer cachexia. In addition, ROS is involved in obesity and muscle insulin resistance, both of which are causally related to type 2 diabetes. A detailed description of the fine-tuning of ROS (including all sources of ROS) in skeletal muscle in health and disease will significantly contribute to our knowledge of both muscle adaptation and muscle related pathologies.
AB - Reactive Oxygen Species (ROS) have been profusely studied as agents of potential damage to living cells and they have been related to a number of pathological processes. Increasing evidence points to a more positive role of ROS in cell signaling and the detailed mechanism that regulates the precise amount of ROS needed for cell functioning without the deleterious effects of excess ROS still needs to be resolved in detail. In skeletal muscle the main source of ROS during normal functioning appears to be NADPH oxidase 2 (NOX2), which is activated by electrical stimuli (or exercise) through a cascade of events that include ATP release through pannexin1 channels. NOX2 is a protein complex that assembles in the T-tubule membrane before activation and ROS production by NOX2 appears to be important for muscle adaptation through gene expression and mitochondrial biogenesis as well as for improving glucose transport after insulin action. Excess ROS production (or diminished antioxidant defenses) plays a role in a number of pathological processes in skeletal muscle. Together with increased reactive nitrogen species, an increase in ROS appears to have a deleterious role in a model of Duchenne muscular dystrophy as well as muscle wasting in other diseases such as aging sarcopenia and cancer cachexia. In addition, ROS is involved in obesity and muscle insulin resistance, both of which are causally related to type 2 diabetes. A detailed description of the fine-tuning of ROS (including all sources of ROS) in skeletal muscle in health and disease will significantly contribute to our knowledge of both muscle adaptation and muscle related pathologies.
KW - Inflammation
KW - Muscle wasting
KW - Muscular dystrophy
KW - NADPH oxidase
KW - Obesity
KW - Sarcopenia
KW - Type 2 diabetes
U2 - 10.1016/j.ceca.2016.02.010
DO - 10.1016/j.ceca.2016.02.010
M3 - Review
C2 - 26965208
AN - SCOPUS:84959564478
VL - 60
SP - 172
EP - 179
JO - Cell Calcium
JF - Cell Calcium
SN - 0143-4160
IS - 3
ER -
ID: 306300730