Mitochondrial and Redox-Based Therapeutic Strategies in Huntington's Disease-Reference-Cited by-同舟云学术

Mitochondrial and Redox-Based Therapeutic Strategies in Huntington's Disease

Published:2021-03-10 Issue:8 Volume:34 Page:650-673
ISSN:1523-0864
Container-title:Antioxidants & Redox Signaling
language:en
Short-container-title:Antioxidants & Redox Signaling

Author:

Fão Lígia¹²³,Rego Ana Cristina¹²³

Affiliation:

1. Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Coimbra, Portugal.

2. Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

3. CIBB-Center for Innovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal.

Publisher

Mary Ann Liebert Inc

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry,Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry

Link

https://www.liebertpub.com/doi/pdf/10.1089/ars.2019.8004

Reference212 articles.

1. Brain mitochondrial iron accumulates in Huntington's disease, mediates mitochondrial dysfunction, and can be removed pharmacologically

2. Role of Rho Kinase Inhibition in the Protective Effect of Fasudil and Simvastatin Against 3-Nitropropionic Acid-Induced Striatal Neurodegeneration and Mitochondrial Dysfunction in Rats

3. Juvenile Huntington’s Disease Skin Fibroblasts Respond with Elevated Parkin Level and Increased Proteasome Activity as a Potential Mechanism to Counterbalance the Pathological Consequences of Mutant Huntingtin Protein

4. FK506 prevents mitochondrial-dependent apoptotic cell death induced by 3-nitropropionic acid in rat primary cortical cultures

5. BDNF regulates BIM expression levels in 3-nitropropionic acid-treated cortical neurons

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