Double-edged alliance: mitochondrial surveillance by the UPS and autophagy.
Mitochondria provide an essential role in the maintenance of cellular homeostasis with regard to energy generation, redox signaling, and programmed cell death. Consequently, fast adaptation to metabolic changes associated with developmental demands or stress induction requires a balanced coordination of mitochondrial biogenesis and removal of damaged mitochondria. Impaired mitochondrial maintenance is causally linked to many human pathologies and aging, including diabetes, cancer, and neurodegenerative diseases. Thus, it is of fundamental importance to understand cellular surveillance mechanisms that support a healthy mitochondrial network. In this review, we discuss the role of ubiquitin-dependent protein degradation in mitochondrial functionality.
Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.
André
A
Franz
Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.
Éva
É
Kevei
Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany. Electronic address: thorsten.hoppe@uni-koeln.de.
Thorsten
T
Hoppe
D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism*; D025801:Ubiquitin / Q000378:metabolism*
D025801:Ubiquitin; D046988:Proteasome Endopeptidase Complex