Abstract
Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. Autophagy is implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role of autophagy as a crucial mediator has been clarified and expanded in the pathological response to redox signalling. Autophagy is a major sensor of the redox signalling. Reactive oxygen species (ROS) are highly reactive molecules that are generated as by-products of cellular metabolism, principally by mitochondria. Mitochondrial ROS (mROS) are beneficial or detrimental to cells depending on their concentration and location. mROS function as redox messengers in intracellular signalling at physiologically low level, whereas excessive production of mROS causes oxidative damage to cellular constituents and thus incurs cell death. Hence, the balance of autophagy-related stress adaptation and cell death is important to comprehend redox signalling-related pathogenesis. In this review, we attempt to provide an overview the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathology.
Highlights
Autophagy was first introduced by Christian de Duve in 1963 as a lysosome-mediated disposal process [1]
Reactive oxygen species (ROS) can act as signalling molecules at the physiological level, which contribute to various cellular processes, including proliferation, differentiation, programmed cell death, innate immunity, autophagy, redox signalling, calcium homeostasis, hypoxic stress responses and stem cell reprogramming [19,20,21,22,23,24,25]
Autophagy eliminates invading pathogens via a selective pathway xenophagy in response to various types of infections [275]. The adapter proteins such as nuclear dot protein 52 kDa (NDP52), optineurin and p62 are involved in xenophagy, which bind to the ubiquitinated proteins and further guide the autophagic proteins [276]
Summary
Autophagy (self-eating) was first introduced by Christian de Duve in 1963 as a lysosome-mediated disposal process [1]. Autophagy is a catabolic process that is essential for cellular homeostasis through the removal of cellular molecules, such as protein aggregates and damaged organelles, via lysosomal digestion [2,3] It regulates the balance between organelle biogenesis, protein synthesis and the clearance of cells [4], which is involved in cellular remodelling during development and differentiation [5]. Autophagy has emerged as a critical mediator of pathological responses is associated with reactive oxygen species (ROS) in both cellular signalling and damage [7]. ROS can act as signalling molecules at the physiological level, which contribute to various cellular processes, including proliferation, differentiation, programmed cell death, innate immunity, autophagy, redox signalling, calcium homeostasis, hypoxic stress responses and stem cell reprogramming [19,20,21,22,23,24,25]. We discuss the effect of autophagy on mitochondrial function and relevance to chronic pathologies
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