What is Autophagy? Definition, Benefits, Ways to Increase It

Autophagy is the process by which our cells recycle their components. Most of the time it runs quietly in the background, but when cells are stressed, autophagy becomes more important. Read on to learn about autophagy, its definition and how it works, autophagy regulation, and what factors increase it.

What is Autophagy?

Autophagy (from the Greek for self-eating) is the regulated process by which a cell degrades its dysfunctional or foreign components. The cell can then recycle useful chemical components for further purposes [1].

This allows autophagy to regulate the balance of protein composition in a cell, prevent the buildup of toxic waste products, maintain cellular organelle function, remove invading pathogens, and sustain cells during periods of low energy input due to fasting or starvation [2].

The scientific importance of understanding autophagy was highlighted when Yoshinori Ohsumi won the 2016 Nobel Prize in Physiology or Medicine for his discoveries of the mechanisms for autophagy.

Mechanism of Autophagy

Essentially, autophagy is the creation of a ‘garbage bag’ (autophagosome) that collects cellular components and then takes them to the cell’s ‘recycling center’ (lysosome) to be broken down into their parts which can then be recycled into new components.

Autophagy-related genes (ATG) are responsible for producing the structures that carry out autophagy. The VPS34 complex initiates the autophagosome, ATG9 contributes to its expansion, and the ATG12-ATG5ATG16L1 complex recruits ATG8 proteins which complete formation and are involved in targeted capture [3].

Other genes are involved in turning autophagy on and off. These genes can detect changes in the cell. mTOR responds to the level of nutrients in a cell and decreases autophagy (by disrupting ULK1 preventing the formation of the VPS34 complex) when there are plenty of nutrients available. AMPK monitors the energy levels in a cell (the amount of ATP) and activates autophagy when they are low. HIF1A detects oxygen levels and turns on autophagy (targeting mitochondria) when they are low (hypoxia) [4, 5].

Sirtuin genes (activated by resveratrol) can inhibit mTOR which increases autophagy [6]. Low levels of NAD+ are also reported to increase autophagy [7].

Research Limitations

Unfortunately, the mechanisms of autophagy are extremely difficult to study in humans, so the vast majority of research discussed in this post was undertaken in animals and cells. This lack of clinical evidence means that very few conclusions can be reliably drawn about autophagy and human health.

The Purpose