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Autophagy (self-eating) in general is viewed as a degradation process which removes non-essential or damaged cellular constituents. » MiPNet article

Reference: Green_2011_Science

Mitochondrial mitophagy

Publications in the MiPMap
Pesta D (2012) Mitochondrial mitophagy. Mitochondr Physiol Network 2012-05-22.

Pesta D (2012) MiPNet

Abstract: A brief accout of mitochondrial mitophagy.

O2k-Network Lab: AT Innsbruck Gnaiger E, DE Cologne Pesta D

Labels: MiParea: mt-Structure;fission;fusion 

HRR: Theory 


Mitophagy, which is specifically targeted to mitochondria, eliminates dysfunctional or damaged mitochondria. During the course of life, mitochondrial genomes accumulate mutations that impair respiration and can lead to excessive formation of reactive oxygen species (ROS). ROS is also a well-known side product of normal respiration and can damage other organelles. By eliminating damaged or dysfunctional components of the cell and the mitochondrion, mitophagy is an important mechanism in the cellular adaptation to stress and serves as a quality-control ensuring proper mitochondrial and cell function.


Autophagy, or in mitochondrial terms, mitophagy occurs by the formation of autophagosomes. These essentially double-membraned vesicles sequester damaged organelles, proteins, or portions of the cytoplasm, which then fuse with lysosomes. After being fused, the sequestered contents are degraded by the acidic environment of lysosomal enzymes. In order to accomplish this task, more than 30 Atg (AuTophaGy-related) proteins are recruited.