Mitochondrial biogenesis as a therapeutic target for traumatic and neurodegenerative CNS diseases.
Alzheimer’s disease
Mitochondrial biogenesis
Mitochondrial dynamics
Mitochondrial dysfunction
Mitophagy
Neuroinflammation
Parkinson’s disease
Spinal cord injury
Stroke
Traumatic brain injury
Journal
Experimental neurology
ISSN: 1090-2430
Titre abrégé: Exp Neurol
Pays: United States
ID NLM: 0370712
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
09
12
2019
revised:
31
03
2020
accepted:
10
04
2020
pubmed:
15
4
2020
medline:
29
12
2020
entrez:
15
4
2020
Statut:
ppublish
Résumé
Central nervous system (CNS) diseases, both traumatic and neurodegenerative, are characterized by impaired mitochondrial bioenergetics and often disturbed mitochondrial dynamics. The dysregulation observed in these pathologies leads to defective respiratory chain function and reduced ATP production, thereby promoting neuronal death. As such, attenuation of mitochondrial dysfunction through induction of mitochondrial biogenesis (MB) is a promising, though still underexplored, therapeutic strategy. MB is a multifaceted process involving the integration of highly regulated transcriptional events, lipid membrane and protein synthesis/assembly and replication of mtDNA. Several nuclear transcription factors promote the expression of genes involved in oxidative phosphorylation, mitochondrial import and export systems, antioxidant defense and mitochondrial gene transcription. Of these, the nuclear-encoded peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is the most commonly studied and is widely accepted as the 'master regulator' of MB. Several recent preclinical studies document that reestablishment of mitochondrial homeostasis through increased MB results in inhibited injury progression and increased functional recovery. This perspective will briefly review the role of mitochondrial dysfunction in the propagation of CNS diseases, while also describing current research strategies that mediate mitochondrial dysfunction and compounds that induce MB for the treatment of acute and chronic neuropathologies.
Identifiants
pubmed: 32289315
pii: S0014-4886(20)30140-0
doi: 10.1016/j.expneurol.2020.113309
pmc: PMC7735537
mid: NIHMS1607129
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
113309Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM084147
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI068021
Pays : United States
Organisme : BLRD VA
ID : I01 BX004868
Pays : United States
Organisme : NIA NIH HHS
ID : T32 AG061897
Pays : United States
Organisme : BLRD VA
ID : I01 BX000851
Pays : United States
Informations de copyright
Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Declaration of Competing Interest No disclosures or competing interests.
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