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Andreas N. Kavazis

Researcher at University of Michigan

Publications -  133
Citations -  6184

Andreas N. Kavazis is an academic researcher from University of Michigan. The author has contributed to research in topics: Skeletal muscle & Oxidative stress. The author has an hindex of 35, co-authored 115 publications receiving 5348 citations. Previous affiliations of Andreas N. Kavazis include Edward Via College of Osteopathic Medicine & University of Florida.

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Journal ArticleDOI

Oxidative stress and disuse muscle atrophy

TL;DR: An overview of muscle proteases, outline intracellular sources of reactive oxygen species, and summarize the evidence that connects oxidative stress to signaling pathways contributing to disuse muscle atrophy are provided.
Journal ArticleDOI

Reactive oxygen species are signalling molecules for skeletal muscle adaptation

TL;DR: This review discusses the redox‐sensitive signalling pathways that are responsible for ROS‐induced skeletal muscle adaptation and discusses the evidence that connects redox signalling to skeletal muscle adaptations in response to increased muscular activity and during prolonged periods of muscular inactivity.
OtherDOI

Reactive oxygen species: Impact on skeletal muscle

TL;DR: Ongoing research continues to explore the redox-sensitive targets in muscle that are responsible for both redox regulation of muscle adaptation and oxidant-mediated muscle fatigue.
Journal ArticleDOI

Mechanisms of disuse muscle atrophy: role of oxidative stress

TL;DR: This review will address the role of reactive oxygen species and oxidative stress as potential contributors to the process of disuse-mediated muscle atrophy, and highlight gaps in knowledge relative to the specific role of oxidative stress in the regulation of disuses.
Journal ArticleDOI

Mitochondria-targeted antioxidants protect against mechanical ventilation-induced diaphragm weakness.

TL;DR: Results reveal that prevention of mechanical ventilation-induced increases in diaphragmatic mitochondrial reactive oxygen species emission protects the diphragm from mechanical ventilation -induced diaphagmatic weakness, and indicates that mitochondria are a primary source of reactive oxygen Species production in the diaphragem during prolonged mechanical ventilation.