Dear Colleagues,

Reactive oxygen species (ROS) play a dual role, as both deleterious and beneficial species. Indeed, ROS function as signalling molecules to mediate physiological responses, such as gene expression, cell proliferation and migration, as well as pathological responses, such as cellular senescence and apoptosis. ROS levels are determined by the balance between ROS generating systems, such as NADPH oxidase and mitochondria, as well as antioxidant defences, such as superoxide dismutase, catalase, and glutathione peroxidase. ROS are associated with metabolic diseases and aging, which are altered by the impairment of redox balance. ROS-mediated cell signalling (redox signalling) is primarily mediated through protein thiol oxidation and their dysregulations contribute to the development of metabolic, inflammation and age-related diseases such as diabetes mellitus, metabolic syndromes, atherosclerosis, and neurodegenerative diseases. Thus, understanding of specific sources of ROS production and how ROS signaling influences metabolic responses, such as mitochondria function, autophagy, metabolic gene expression, proteasome responses and inflammation including senescence-associated secretory phenotype (SASP) may lead to treat metabolic and age-related diseases. Moreover, it is important to identify the biological and (patho)physiological consequences of oxidative protein modifications and understand how they integrate and cross-talk with other signalling events in these diseases, which will develop therapeutic targets.

This Special Issue calls for papers coming from all over the world. Original studies, up-to-date/comprehensive review articles, and commentaries are all welcome.

Prof. Dr. Masuko Ushio-Fukai
Guest Editor

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• reactive oxygen species
• redox signaling
• metabolic disease
• aging
• NADPH oxidase
• mitochondria
• antioxidants
• thiol oxidation
• inflammation