ReviewMolecular neurobiology2016
Mutant Huntingtin and Elusive Defects in Oxidative Metabolism and Mitochondrial Calcium Handling.
Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Huntingtin loss in hepatocytes is associated with altered metabolism, adhesion, and liver zonation.Life science alliance · 2023Article
- Genome-wide screening in pluripotent cells identifies Mtf1 as a suppressor of mutant huntingtin toxicity.Nature communications · 2023Article
- Huntingtin loss in hepatocytes is associated with altered metabolism, adhesion, and liver zonation.bioRxiv : the preprint server for biology · 2023Article
- Oxidative Stress and Antioxidants in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2023Review
- Recent approaches on Huntington's disease (Review).Biomedical reports · 2023Review
- Review
- Review
- Mitochondrial CaCells · 2021Review
- Mutant huntingtin does not cross the mitochondrial outer membrane.Human molecular genetics · 2020Article
- How Do Post-Translational Modifications Influence the Pathomechanistic Landscape of Huntington's Disease? A Comprehensive Review.International journal of molecular sciences · 2020Review
- Energy Metabolism and Mitochondrial Superoxide Anion Production in Pre-symptomatic Striatal Neurons Derived from Human-Induced Pluripotent Stem Cells Expressing Mutant Huntingtin.Molecular neurobiology · 2020Article
- Dysfunction of Mitochondrial CaFrontiers in cell and developmental biology · 2020Review
- The Role of Exosomal microRNAs and Oxidative Stress in Neurodegenerative Diseases.Oxidative medicine and cellular longevity · 2020Review
- Mutant huntingtin fails to directly impair brain mitochondria.Journal of neurochemistry · 2019Article
- Metabolic Reprogramming in Astrocytes Distinguishes Region-Specific Neuronal Susceptibility in Huntington Mice.Cell metabolism · 2019Article
- Carnosic Acid as a Promising Agent in Protecting Mitochondria of Brain Cells.Molecular neurobiology · 2018Review
- Huntington Disease as a Neurodevelopmental Disorder and Early Signs of the Disease in Stem Cells.Molecular neurobiology · 2018Review
- A Mitochondria-Associated Oxidative Stress Perspective on Huntington's Disease.Frontiers in molecular neuroscience · 2018Review
- Oxidative metabolism and CaNeurochemistry international · 2017Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Elongation of a polyglutamine (polyQ) stretch in huntingtin protein (Htt) is linked to Huntington's disease (HD) pathogenesis. The mutation in Htt correlates with neuronal dysfunction in the striatum and cerebral cortex and eventually leads to neuronal cell death. The exact mechanisms of the injurious effect of mutant Htt (mHtt) on neurons are not completely understood but might include aberrant gene transcription, defective autophagy, abnormal mitochondrial biogenesis, anomalous mitochondrial dynamics, and trafficking. In addition, deficiency in oxidative metabolism and defects in mitochondrial Ca(2+) handling are considered essential contributing factors to neuronal dysfunction in HD and, consequently, in HD pathogenesis. Since the discovery of the mutation in Htt, the questions whether mHtt affects oxidative metabolism and mitochondrial Ca(2+) handling and, if it does, what mechanisms could be involved were in focus of numerous investigations. However, despite significant research efforts, the detrimental effect of mHtt and the mechanisms by which mHtt might impair oxidative metabolism and mitochondrial Ca(2+) handling remain elusive. In this paper, I will briefly review studies aimed at clarifying the consequences of mHtt interaction with mitochondria and discuss experimental results supporting or arguing against the mHtt effects on oxidative metabolism and mitochondrial Ca(2+) handling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.