Mitochondrial Quality Control Proteases in Neuronal Welfare

Roman M. Levytskyy, Edward M. Germany, Oleh Khalimonchuk

Research output: Contribution to journalReview article

14 Citations (Scopus)

Abstract

The functional integrity of mitochondria is a critical determinant of neuronal health and compromised mitochondrial function is a commonly recognized factor that underlies a plethora of neurological and neurodegenerative diseases. Metabolic demands of neural cells require high bioenergetic outputs that are often associated with enhanced production of reactive oxygen species. Unopposed accumulation of these respiratory byproducts over time leads to oxidative damage and imbalanced protein homeostasis within mitochondrial subcompartments, which in turn may result in cellular demise. The post-mitotic nature of neurons and their vulnerability to these stress factors necessitate strict protein homeostatic control to prevent such scenarios. A series of evolutionarily conserved proteases is one of the central elements of mitochondrial quality control. These versatile proteolytic enzymes conduct a multitude of activities to preserve normal mitochondrial function during organelle biogenesis, metabolic remodeling and stress. In this review we discuss neuroprotective aspects of mitochondrial quality control proteases and neuropathological manifestations arising from defective proteolysis within the mitochondrion.

Original languageEnglish (US)
Pages (from-to)629-644
Number of pages16
JournalJournal of Neuroimmune Pharmacology
Volume11
Issue number4
DOIs
StatePublished - Dec 1 2016

Fingerprint

Quality Control
Peptide Hydrolases
Mitochondria
Organelle Biogenesis
Neurodegenerative Diseases
Energy Metabolism
Proteolysis
Reactive Oxygen Species
Proteins
Homeostasis
Neurons
Health

Keywords

  • Hereditary neurological diseases
  • Mitochondria
  • Mitochondrial proteases
  • Mitochondrial quality control
  • Neurodegenerative diseases
  • Neurons

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Immunology and Allergy
  • Immunology
  • Pharmacology

Cite this

Mitochondrial Quality Control Proteases in Neuronal Welfare. / Levytskyy, Roman M.; Germany, Edward M.; Khalimonchuk, Oleh.

In: Journal of Neuroimmune Pharmacology, Vol. 11, No. 4, 01.12.2016, p. 629-644.

Research output: Contribution to journalReview article

Levytskyy, Roman M. ; Germany, Edward M. ; Khalimonchuk, Oleh. / Mitochondrial Quality Control Proteases in Neuronal Welfare. In: Journal of Neuroimmune Pharmacology. 2016 ; Vol. 11, No. 4. pp. 629-644.
@article{800df0419d0840d4a9a4a07b4f85625b,
title = "Mitochondrial Quality Control Proteases in Neuronal Welfare",
abstract = "The functional integrity of mitochondria is a critical determinant of neuronal health and compromised mitochondrial function is a commonly recognized factor that underlies a plethora of neurological and neurodegenerative diseases. Metabolic demands of neural cells require high bioenergetic outputs that are often associated with enhanced production of reactive oxygen species. Unopposed accumulation of these respiratory byproducts over time leads to oxidative damage and imbalanced protein homeostasis within mitochondrial subcompartments, which in turn may result in cellular demise. The post-mitotic nature of neurons and their vulnerability to these stress factors necessitate strict protein homeostatic control to prevent such scenarios. A series of evolutionarily conserved proteases is one of the central elements of mitochondrial quality control. These versatile proteolytic enzymes conduct a multitude of activities to preserve normal mitochondrial function during organelle biogenesis, metabolic remodeling and stress. In this review we discuss neuroprotective aspects of mitochondrial quality control proteases and neuropathological manifestations arising from defective proteolysis within the mitochondrion.",
keywords = "Hereditary neurological diseases, Mitochondria, Mitochondrial proteases, Mitochondrial quality control, Neurodegenerative diseases, Neurons",
author = "Levytskyy, {Roman M.} and Germany, {Edward M.} and Oleh Khalimonchuk",
year = "2016",
month = "12",
day = "1",
doi = "10.1007/s11481-016-9683-8",
language = "English (US)",
volume = "11",
pages = "629--644",
journal = "Journal of NeuroImmune Pharmacology",
issn = "1557-1890",
publisher = "Springer New York",
number = "4",

}

TY - JOUR

T1 - Mitochondrial Quality Control Proteases in Neuronal Welfare

AU - Levytskyy, Roman M.

AU - Germany, Edward M.

AU - Khalimonchuk, Oleh

PY - 2016/12/1

Y1 - 2016/12/1

N2 - The functional integrity of mitochondria is a critical determinant of neuronal health and compromised mitochondrial function is a commonly recognized factor that underlies a plethora of neurological and neurodegenerative diseases. Metabolic demands of neural cells require high bioenergetic outputs that are often associated with enhanced production of reactive oxygen species. Unopposed accumulation of these respiratory byproducts over time leads to oxidative damage and imbalanced protein homeostasis within mitochondrial subcompartments, which in turn may result in cellular demise. The post-mitotic nature of neurons and their vulnerability to these stress factors necessitate strict protein homeostatic control to prevent such scenarios. A series of evolutionarily conserved proteases is one of the central elements of mitochondrial quality control. These versatile proteolytic enzymes conduct a multitude of activities to preserve normal mitochondrial function during organelle biogenesis, metabolic remodeling and stress. In this review we discuss neuroprotective aspects of mitochondrial quality control proteases and neuropathological manifestations arising from defective proteolysis within the mitochondrion.

AB - The functional integrity of mitochondria is a critical determinant of neuronal health and compromised mitochondrial function is a commonly recognized factor that underlies a plethora of neurological and neurodegenerative diseases. Metabolic demands of neural cells require high bioenergetic outputs that are often associated with enhanced production of reactive oxygen species. Unopposed accumulation of these respiratory byproducts over time leads to oxidative damage and imbalanced protein homeostasis within mitochondrial subcompartments, which in turn may result in cellular demise. The post-mitotic nature of neurons and their vulnerability to these stress factors necessitate strict protein homeostatic control to prevent such scenarios. A series of evolutionarily conserved proteases is one of the central elements of mitochondrial quality control. These versatile proteolytic enzymes conduct a multitude of activities to preserve normal mitochondrial function during organelle biogenesis, metabolic remodeling and stress. In this review we discuss neuroprotective aspects of mitochondrial quality control proteases and neuropathological manifestations arising from defective proteolysis within the mitochondrion.

KW - Hereditary neurological diseases

KW - Mitochondria

KW - Mitochondrial proteases

KW - Mitochondrial quality control

KW - Neurodegenerative diseases

KW - Neurons

UR - http://www.scopus.com/inward/record.url?scp=84965029326&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84965029326&partnerID=8YFLogxK

U2 - 10.1007/s11481-016-9683-8

DO - 10.1007/s11481-016-9683-8

M3 - Review article

C2 - 27137937

AN - SCOPUS:84965029326

VL - 11

SP - 629

EP - 644

JO - Journal of NeuroImmune Pharmacology

JF - Journal of NeuroImmune Pharmacology

SN - 1557-1890

IS - 4

ER -