Autophagy is a cellular mechanism which preserves cell health by recycling long-lived proteins and damaged organelles.
With the discovery of its mechanisms by Professor Yoshinori Ohsumi (Nobel Prize in Physiology and Medicine 2016), autophagy has been the subject of intense research interest that revealed its role in various physiological and pathological conditions.
This catabolic pathway consists of multiple sequential steps, promoted through two well-characterised signalling cascades known as mTOR (mammalian Target Of Rapamycin)-dependent and mTOR independent pathways. The process starts with the sequestration of the targeted organelles subject to degradation along with a portion of cytosol into a double-or multimembrane structure known as phagophore. This structure elongates after closure to form a vesicular structure, termed autophagosome. Subsequently, the mature autophagosome fuses with the lysosome, thereby forming a single membrane structure (autolysosome) where protein degradation is promoted by lysosomal enzymes.1,2
Autophagy constitutively occurs at basal cellular level to ensure the homeostatic turnover of cell components but can also be activated in the following conditions: (i) when the cells need to mobilise intracellular nutrients, (ii) when the cells need to clear potentially toxic cytoplasmic materials or (iii) when the cells are under various stress conditions like oxidative stress or radiation.3 Under these circumstances, altered components are degraded to be subsequently replaced by newly produced ones, allowing the cells and organisms to preserve their physiological functions.
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