The emerging roles of nicotinamide adenine dinucleotide phosphate oxidase 2 in skeletal muscle redox signaling and metabolism
Research output: Contribution to journal › Review › Research › peer-review
- Henriquez-Olguin et al_Antioxidants & Redox Signaling_2019_Vol 31(8)_1371-1410
Final published version, 2.2 MB, PDF document
Significance: Skeletal muscle is a crucial tissue to whole-body locomotion and metabolic health. Reactive oxygen species (ROS) have emerged as intracellular messengers participating in both physiological and pathological adaptations in skeletal muscle. A complex interplay between ROS-producing enzymes and antioxidant networks exists in different subcellular compartments of mature skeletal muscle. Recent evidence suggests that NADPH oxidases (NOX) are a major source of contraction- and insulin-stimulated oxidants production, but may paradoxically also contribute to muscle insulin resistance and atrophy.
Recent advances: Pharmacological and molecular biological tools, including redox-sensitive probes and transgenic mouse models, have generated novel insights into compartmentalized redox signaling and suggested that NOX2 contributes to redox control of skeletal muscle metabolism.
Critical issues: Major outstanding questions in skeletal muscle include where NOX2 activation occurs under different conditions in health and disease, how NOX2 activation is regulated, how superoxide/ H2O2 generated by NOX2 reaches the cytosol, what the signaling mediators are downstream of NOX2, and the role of NOX2 for different physiological and pathophysiological processes.
Future directions: Future research should utilize and expand the current redox-signaling toolbox to clarify the NOX2-dependent mechanisms in skeletal muscle and determine whether the proposed functions of NOX2 in cells and animal models are conserved into man.
|Journal||Antioxidants & Redox Signaling|
|Number of pages||40|
|Publication status||Published - 2019|
- Faculty of Science - Exercise, Skeletal muscle, Glucose metabolism, Insulin resistance, Atrophy