Dynamics of redox signaling in aging via autophagy, inflammation, and senescence.

Abstract

Review paper attempts to explain the dynamic aspects of redox signaling in aging through autophagy, inflammation, and senescence. It begins with ROS source in the cell, then states redox signaling in autophagy, and regulation of autophagy in aging. Next, we discuss inflammation and redox signaling with various pathways involved: NOX pathway, ROS production via TNF-α, IL-1β, xanthine oxidase pathway, COX pathway, and myeloperoxidase pathway. Also, we emphasize oxidative damage as an aging marker and the contribution of pathophysiological factors to aging. In senescence-associated secretory phenotypes, we link ROS with senescence, aging disorders. Relevant crosstalk between autophagy, inflammation, and senescence using a balanced ROS level might reduce age-related disorders. Transducing the context-dependent signal communication among these three processes at high spatiotemporal resolution demands other tools like multi-omics aging biomarkers, artificial intelligence, machine learning, and deep learning. The bewildering advancement of technology in the above areas might progress age-related disorders diagnostics with precision and accuracy.