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Definition: How can autophagy be induced in response to cellular stress?

In response to cellular stress, such as nutrient deprivation, oxidative stress, or pathogen invasion, autophagy can be induced as a protective response. The induction of autophagy helps to remove damaged proteins, organelles, and other cellular debris, thereby promoting cell survival and preventing the accumulation of toxic substances.

There are several ways in which autophagy can be induced in response to cellular stress:

1. mTOR inhibition: The mammalian target of rapamycin (mTOR) is a key regulator of autophagy. Inhibition of mTOR signaling, either through nutrient deprivation or the use of specific inhibitors, can trigger autophagy.

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2. AMPK activation: AMP-activated protein kinase (AMPK) is a cellular energy sensor that is activated under conditions of low energy availability. AMPK activation can stimulate autophagy by phosphorylating and activating key autophagy-related proteins.

3. ER stress: Endoplasmic reticulum (ER) stress, caused by the accumulation of misfolded proteins, can induce autophagy as a protective response. ER stress sensors, such as PERK, IRE1, and ATF6, can activate autophagy through various signaling pathways.

4. Reactive oxygen species (ROS): Increased levels of reactive oxygen species (ROS) can activate autophagy as a defense mechanism against oxidative stress. ROS can directly modulate autophagy-related proteins or activate signaling pathways, such as the AMPK pathway, to induce autophagy.

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5. Hypoxia: Oxygen deprivation, or hypoxia, can trigger autophagy as a survival response. Hypoxia-inducible factors (HIFs) can activate autophagy genes and promote autophagosome formation under hypoxic conditions.

In summary, autophagy can be induced in response to cellular stress through various mechanisms, including mTOR inhibition, AMPK activation, ER stress, ROS signaling, and hypoxia. These inducers of autophagy help to maintain cellular homeostasis and promote longevity by removing damaged components and ensuring cellular survival.

Keywords: autophagy, cellular, stress, response, induced, proteins, signaling, activate, hypoxia