Autophagy is a conserved dynamic catabolic process, in which nonfunctional macromolecules and cellular organelles are engulfed, degraded, and recycled, and thereby it plays a crucial role in maintaining cellular homeostasis. A basal level of reactive oxygen species (ROS) is essential for the cell signaling and survival, but their elevated levels have been attributed to multiple pathologies and ageing. ROS induced oxidation is the primary mechanism through which cellular macromolecules accumulate damage over a period of time. Oxidative stress has long been identified to play a central role in the progression of cellular senescence and diabetes. The imbalance in the ROS production has been noted to immediately follow the nutrient deprivation and therefore it represents an important mediator of the autophagy. The cellular organelles such as mitochondria, peroxisome, and endoplasmic reticulum play a critical role in the cellular metabolism and remain at higher risk of accumulating oxidative damage.

In this special issue we invite investigators to contribute their original research, both in vitro and in vivo studies, and/or review article to broaden our understanding of the link between oxidative stress and autophagy process and their role in the regulation of cellular longevity and pathogenesis of metabolic disorders.

Potential topics include, but are not limited to:

• Oxidative stress and autophagy in regulation of longevity and/or metabolism
• Targeting autophagy pathway in diabetes
• Autophagy of cellular organelles such as mitochondria and peroxisome in the regulation of cellular longevity and/or metabolic disorder such as diabetes
• Identification of biomarkers allowing monitoring of physiological or pathophysiological events regulating progression of metabolic disorders and/or longevity
• Role of autophagy and oxidant signaling in the nutrient deprivation/caloric restriction mediated beneficial effects in metabolic disorders and ageing
• Selective autophagy in regulation of cellular longevity