ReviewMolecular neurobiology2019
Disease Modeling and Therapeutic Strategies in CMT2A: State of the Art.
Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- MFN2 coordinates mitochondria motility with α-tubulin acetylation and this regulation is disrupted in CMT2A.iScience · 2024Article
- Charcot-Marie-Tooth type 2A in vivo models: Current updates.Journal of cellular and molecular medicine · 2024Review
- Hereditary Optic Neuropathies: A Systematic Review on the Interplay between Biomaterials and Induced Pluripotent Stem Cells.Bioengineering (Basel, Switzerland) · 2024Review
- E4 ubiquitin ligase promotes mitofusin turnover and mitochondrial stress response.Molecular cell · 2023Article
- Docking and stability defects in mitofusin highlight the proteasome as a potential therapeutic target.iScience · 2023Article
- Review
- Mitochondrial dynamics proteins as emerging drug targets.Trends in pharmacological sciences · 2023Review
- Multiple respiratory complications in a patient with Charcot-Marie-Tooth disease with MFN2 mutation.Respiratory medicine case reports · 2022Article
- Animal Models of CMT2A: State-of-art and Therapeutic Implications.Molecular neurobiology · 2020Review
- Targeting the programmed axon degeneration pathway as a potential therapeutic for Charcot-Marie-Tooth disease.Brain research · 2020Review
- Role of Mitofusins and Mitophagy in Life or Death Decisions.Frontiers in cell and developmental biology · 2020Review
- Dual role of a GTPase conformational switch for membrane fusion by mitofusin ubiquitylation.Life science alliance · 2020Article
- Plasticity in salt bridge allows fusion-competent ubiquitylation of mitofusins and Cdc48 recognition.Life science alliance · 2019Article
- Mitochondrial dynamics and their potential as a therapeutic target.Mitochondrion · 2019Review
- Charcot-Marie-Tooth: From Molecules to Therapy.International journal of molecular sciences · 2019Review
- Mitofusins: Disease Gatekeepers and Hubs in Mitochondrial Quality Control by E3 Ligases.Frontiers in physiology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mitofusin 2 (MFN2) is a protein of the mitochondrial outer membrane that belongs to a family of highly conserved dynamin-related GTPases. It is implicated in several intracellular pathways; however, its main role is the regulation of mitochondrial dynamics, in particular mitochondrial fusion. Mutations in MFN2 are associated with Charcot-Marie-Tooth disease type 2A (CMT2A), a neurological disorder characterized by a wide spectrum of clinical features, primarily a motor sensory neuropathy. The cellular and molecular mechanisms by which MFN2 mutations lead to neuronal degeneration are largely unknown, and there is currently no cure for patients. Here, we present the most recent in vitro and in vivo models of CMT2A and the more promising therapeutic approaches under development. These models and therapies may represent relevant tools for the study and recovery of defective mitochondrial dynamics that seem to play a significant role in the pathogenesis of other more common neurodegenerative diseases.
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What OpenQuestion holds
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.