Neurodegeneration as a consequence of failed mitochondrial maintenance
- PMID: 22143516
- DOI: 10.1007/s00401-011-0921-0
Neurodegeneration as a consequence of failed mitochondrial maintenance
Abstract
Maintaining the functional integrity of mitochondria is pivotal for cellular survival. It appears that neuronal homeostasis depends on high-fidelity mitochondria, in particular. Consequently, mitochondrial dysfunction is a fundamental problem associated with a significant number of neurological diseases, including Parkinson's disease (PD), Huntington's disease (HD), Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS) and various peripheral neuropathies, as well as the normal aging process. To ensure optimal mitochondrial function, diverse, evolutionarily conserved mitochondrial quality control mechanisms are in place, including the scavenging of toxic reactive oxygen species (ROS) and degradation of damaged mitochondrial proteins, but also turnover of whole organelles. In this review we will discuss various mitochondria-associated conditions, focusing on the role of protein turnover in mitochondrial maintenance with special emphasis on neurodegenerative disorders.
Similar articles
-
Dynamin-related protein 1 and mitochondrial fragmentation in neurodegenerative diseases.Brain Res Rev. 2011 Jun 24;67(1-2):103-18. doi: 10.1016/j.brainresrev.2010.11.004. Epub 2010 Dec 8. Brain Res Rev. 2011. PMID: 21145355 Free PMC article. Review.
-
Mitochondrial protein import dysfunction: mitochondrial disease, neurodegenerative disease and cancer.FEBS Lett. 2021 Apr;595(8):1107-1131. doi: 10.1002/1873-3468.14022. Epub 2021 Jan 28. FEBS Lett. 2021. PMID: 33314127 Review.
-
Oxidative stress, mitochondrial dysfunction and cellular stress response in Friedreich's ataxia.J Neurol Sci. 2005 Jun 15;233(1-2):145-62. doi: 10.1016/j.jns.2005.03.012. J Neurol Sci. 2005. PMID: 15896810 Review.
-
mtDNA Maintenance and Alterations in the Pathogenesis of Neurodegenerative Diseases.Curr Neuropharmacol. 2023;21(3):578-598. doi: 10.2174/1570159X20666220810114644. Curr Neuropharmacol. 2023. PMID: 35950246 Free PMC article. Review.
-
Less than perfect divorces: dysregulated mitochondrial fission and neurodegeneration.Acta Neuropathol. 2012 Feb;123(2):189-203. doi: 10.1007/s00401-011-0930-z. Epub 2011 Dec 17. Acta Neuropathol. 2012. PMID: 22179580 Review.
Cited by
-
Mitophagy in hypertension-mediated organ damage.Front Cardiovasc Med. 2024 Jan 4;10:1309863. doi: 10.3389/fcvm.2023.1309863. eCollection 2023. Front Cardiovasc Med. 2024. PMID: 38239871 Free PMC article. Review.
-
Astrocytes of the eye and optic nerve: heterogeneous populations with unique functions mediate axonal resilience and vulnerability to glaucoma.Front Ophthalmol (Lausanne). 2023;3:1217137. doi: 10.3389/fopht.2023.1217137. Epub 2023 Jul 21. Front Ophthalmol (Lausanne). 2023. PMID: 37829657 Free PMC article.
-
Sublethal toxicities of 2,4-dinitrophenol as inferred from online self-reports.PLoS One. 2023 Sep 13;18(9):e0290630. doi: 10.1371/journal.pone.0290630. eCollection 2023. PLoS One. 2023. PMID: 37703241 Free PMC article.
-
Glial Activation, Mitochondrial Imbalance, and Akt/mTOR Signaling May Be Potential Mechanisms of Cognitive Impairment in Heart Failure Mice.Neurotox Res. 2023 Dec;41(6):589-603. doi: 10.1007/s12640-023-00655-2. Epub 2023 Sep 5. Neurotox Res. 2023. PMID: 37668877
-
Post-translational modifications and protein quality control of mitochondrial channels and transporters.Front Cell Dev Biol. 2023 Aug 3;11:1196466. doi: 10.3389/fcell.2023.1196466. eCollection 2023. Front Cell Dev Biol. 2023. PMID: 37601094 Free PMC article. Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Miscellaneous
