Autophagy

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Autophagy is an essential cellular process, used by cells to degrade damaged and unneccessary cytosolic macromolecules and organelles, for example proteins. This prevents cell functions and pathways from being damaged or interrupted by aggregates of proteins or non-functioning organelles, a key cause of disease. Autophagy proceeds via a five-step mechanism that starts with the sequestration of cytosolic material by a double-membrane, known as a 'phagophore'.  

One of the key products of autophagy, amino acids, can be used for anabolic processes within the cell.

Autophagy is controlled by mTOR (Mechanistic target of rapomycin), a kinase coded for by the MTOR gene. When mTOR is activated, autophagy is suppressed. mTOR can be suppressed by low amino acid concentrations, allowing autophagy to produce more amino acids.[1][2]

=== The cellular mechanism autophagy is required in the recycling of nutrients contained within cells for use in
pathways or regeneration of cells and organelles. Autophagy is referred to as 'self-eating' the autophagosome hydrolyses organelles/


cellular structures within the cell; hydrolytic enzymes digest the organelle and its contents via the use of hydrolytic enzymes [1]. An


autophagosome in order to destroy the targeted structure, the enclosing membrane (which forms the autophagosomic vacuole) forms


from the endoplasmic recticulum [1]. These target structures aren't required; due to damage, infection, or age (i.e. red blood


cells are destroyed after 120 days, as they are in a continous cycle being replaced with new red blood cells). Autophagy is important


celluar mechanism as it supplies the cell with everything it requires to function (i.e. amino acids, sugars etc) [2]. Autophagy prevents


further damage occurring to the cell/ tissues by removing harmful molecules and preventing their accumulation. It is extremely prominent


in the case of starving cells where nutrients are required for other cells, therefore cells are destroyed to produce nutrients to supply


normal somatic cells with the nutrients they require.

===

Contents

References

  1. Lin S., Leng Z., Guo Y., Cai L., Cai Y., Li N., Shang H., Le W., Zhao W., Wu Z. (2015). Suppression of mTOR pathway and induction of autophagy-dependent cell death by cabergoline. Oncotarget, 5744 (Epub ahead of print)
  2. Carroll, B., Korolchuk, V., Sarkar, S. (2015). Amino acids and autophagy: cross-talk and co-operation to control cellular homeostasis. Amino Acids, 47(10), pp2065-2088


[1] Hardin J and Bertoni G. Becker’s world of the cell. 9th edition, United States: Pearson Education. 2017

[2] Esposito E, Campolo M, Cordaro M, Casili G and Cuzzocrea S. Autophagy networks in inflammation. switzerland. springer, cham.2016

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