Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 78, Issue 8, Pages 3853-3866Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-021-03775-0
Keywords
Mitochondrial dysfunction; UPRmt; ISR; Mitochondrial fission; Mitochondrial fusion; Mitophagy; PINK1; Parkin; Mitochondrial diseases
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Mitochondria and the nucleus communicate to regulate mitochondrial homeostasis, with mitochondria changing morphology and undergoing degradation through mitophagy in response to external stimuli. Proper function and regulation of these mitochondrial quality control pathways are crucial for cellular homeostasis.
Mitochondria are organelles central to myriad cellular processes. To maintain mitochondrial health, various processes co-operate at both the molecular and organelle level. At the molecular level, mitochondria can sense imbalances in their homeostasis and adapt to these by signaling to the nucleus. This mito-nuclear communication leads to the expression of nuclear stress response genes. Upon external stimuli, mitochondria can also alter their morphology accordingly, by inducing fission or fusion. In an extreme situation, mitochondria are degraded by mitophagy. Adequate function and regulation of these mitochondrial quality control pathways are crucial for cellular homeostasis. As we discuss, alterations in these processes have been linked to several pathologies including neurodegenerative diseases and cancer.
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