While hazardous at high concentrations, free radicals and radical-derived, nonradical reactive species in moderate concentrations play an important role as regulatory mediators in signaling processes. Many of the reactive species-mediated responses actually protect the cells against oxidative stress and re-establish "redox homeostasis”, with molecules such as NO and ROS involved in many physiological functions, acting in higher organisms from the cellular to the systemic level. Redox signaling and homeostasis are understood as a complex network of enzymes, factors, and pathways involved in the generation, neutralization, and response to reactive species, which involves a strict cross-talk between subcellular components and different organ districts, finally regulating cell and whole body metabolism.
In recent decades, many multidisciplinary studies have shown that redox signaling and homeostasis are altered in different cell types and tissues in response to varying physiological and pathological conditions. Modulation signals include hormones, nutrients, exogenous substances such as drugs and endocrine disruptors, alterations in cellular energy status, and conditions such as obesity, insulin resistance, ectopic adiposity (e.g., NAFLD), caloric restriction, and exercise. In a cell and tissue specific manner, redox signaling and homeostasis may involve altered gene expression, mitochondrial functions and dynamics, endoplasmic reticulum stress, and pathways such as autophagy, inflammation, and cell death. Relevant tissues in which alterations in the redox signaling and homeostasis result in effects on the metabolism include the central nervous system, the liver, skeletal muscle, adipose tissues, and endocrine glands.
This Research Topic aims to provide an updated picture of the factors involved in the modulation of metabolism in response to impaired redox signaling and homeostasis in physiological and pathological conditions, highlighting the interplay between central and peripheral districts. Original research, reviews, and mini reviews focusing on the following subjects are of particular interest:
• Redox signaling and homeostasis in obesity: central and peripheral districts
• Mitochondrial energy metabolism and redox signaling in neurodegenerative disease
• Drugs and endocrine disruptors: effects on redox signaling and homeostasis in metabolic dysfunctions
• Redox signaling and homeostasis in the control of autophagy: metabolic effects in central and peripheral districts
• Mitochondrial functions and redox signaling and homeostasis in the control of metabolism
While hazardous at high concentrations, free radicals and radical-derived, nonradical reactive species in moderate concentrations play an important role as regulatory mediators in signaling processes. Many of the reactive species-mediated responses actually protect the cells against oxidative stress and re-establish "redox homeostasis”, with molecules such as NO and ROS involved in many physiological functions, acting in higher organisms from the cellular to the systemic level. Redox signaling and homeostasis are understood as a complex network of enzymes, factors, and pathways involved in the generation, neutralization, and response to reactive species, which involves a strict cross-talk between subcellular components and different organ districts, finally regulating cell and whole body metabolism.
In recent decades, many multidisciplinary studies have shown that redox signaling and homeostasis are altered in different cell types and tissues in response to varying physiological and pathological conditions. Modulation signals include hormones, nutrients, exogenous substances such as drugs and endocrine disruptors, alterations in cellular energy status, and conditions such as obesity, insulin resistance, ectopic adiposity (e.g., NAFLD), caloric restriction, and exercise. In a cell and tissue specific manner, redox signaling and homeostasis may involve altered gene expression, mitochondrial functions and dynamics, endoplasmic reticulum stress, and pathways such as autophagy, inflammation, and cell death. Relevant tissues in which alterations in the redox signaling and homeostasis result in effects on the metabolism include the central nervous system, the liver, skeletal muscle, adipose tissues, and endocrine glands.
This Research Topic aims to provide an updated picture of the factors involved in the modulation of metabolism in response to impaired redox signaling and homeostasis in physiological and pathological conditions, highlighting the interplay between central and peripheral districts. Original research, reviews, and mini reviews focusing on the following subjects are of particular interest:
• Redox signaling and homeostasis in obesity: central and peripheral districts
• Mitochondrial energy metabolism and redox signaling in neurodegenerative disease
• Drugs and endocrine disruptors: effects on redox signaling and homeostasis in metabolic dysfunctions
• Redox signaling and homeostasis in the control of autophagy: metabolic effects in central and peripheral districts
• Mitochondrial functions and redox signaling and homeostasis in the control of metabolism
