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Autophagy is an essential cellular process, used by cells to degrade damaged and unnecessary 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 rapamycin), 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[3]. An autophagosome in order to destroy the targeted structure, the enclosing membrane (which forms the autophagosomic vacuole) forms from the endoplasmic reticulum[[|]][4]. 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 continuous cycle being replaced with new red blood cells). Autophagy is an important cellular mechanism as it supplies the cell with everything it requires to function (i.e. amino acids, sugars etc.)[5]. 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.


  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
  3. Hardin J and Bertoni G. Becker’s world of the cell. 9th edition, United States: Pearson Education. 2017
  4. Hardin J and Bertoni G. Becker’s world of the cell. 9th edition, United States: Pearson Education. 2017
  5. Esposito E, Campolo M, Cordaro M, Casili G and Cuzzocrea S. Autophagy networks in inflammation. switzerland. springer, cham.2016

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