ReviewFrontiers in physiology2020
Mitofusin 2 Dysfunction and Disease in Mice and Men.
Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- HDAC6 inhibition alleviates mitochondrial trafficking in models of Charcot-Marie-Tooth disease type 2A.JCI insight · 2026Article
- Lipodystrophy Syndromes: One Name but Many Diseases Highlighting the Importance of Adipose Tissue in Metabolism.Current diabetes reports · 2025Review
- The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease.Biomolecules · 2025Review
- Loss of nuclear envelope bud formation leads to mitophagy initiation inAutophagy reports · 2025Article
- Sensory-Motor Neuropathy in Mfn2 T105M Knock-in Mice and Its Reversal by a Novel Piperine-Derived Mitofusin Activator.The Journal of pharmacology and experimental therapeutics · 2024Article
- MFN2 coordinates mitochondria motility with α-tubulin acetylation and this regulation is disrupted in CMT2A.iScience · 2024Article
- Massively parallel screen uncovers many rare 3' UTR variants regulating mRNA abundance of cancer driver genes.Nature communications · 2024Article
- Acetate ameliorates ovarian mitochondrial dysfunction in letrozole-induced polycystic ovarian syndrome rat model by improving mitofusin-2.The journal of physiological sciences : JPS · 2024Article
- A case report of peroneal muscle atrophy type 2A2 with central nervous system involvement as initial presentation.BMC pediatrics · 2024Article
- Misregulation of mitochondria-lysosome contact dynamics in Charcot-Marie-Tooth Type 2B disease Rab7 mutant sensory peripheral neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- LRRK2 is involved in the chemotaxis of neutrophils and differentiated HL-60 cells, and the inhibition of LRRK2 kinase activity increases fMLP-induced chemotactic activity.Cell communication and signaling : CCS · 2023Article
- DIAPH1-MFN2 interaction regulates mitochondria-SR/ER contact and modulates ischemic/hypoxic stress.Nature communications · 2023Article
- Role of tubulin post-translational modifications in peripheral neuropathy.Experimental neurology · 2023Review
- A SARM1-mitochondrial feedback loop drives neuropathogenesis in a Charcot-Marie-Tooth disease type 2A rat model.The Journal of clinical investigation · 2022Article
- Mitochondrial Dysfunction and Pharmacodynamics of Mitofusin Activation in Murine Charcot-Marie-Tooth Disease Type 2A.The Journal of pharmacology and experimental therapeutics · 2022Article
- Small molecules that enhance mitophagy to delay aging and neurodegeneration.The journal of cardiovascular aging · 2022Article
- Genotype-phenotype characteristics of Vietnamese patients diagnosed with Charcot-Marie-Tooth disease.Brain and behavior · 2022Article
- 'Fly-ing' from rare to common neurodegenerative disease mechanisms.Trends in genetics : TIG · 2022Review
- Neurohormonal connections with mitochondria in cardiomyopathy and other diseases.American journal of physiology. Cell physiology · 2022Review
- Clinical and genetic features of a cohort of patients with MFN2-related neuropathy.Scientific reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
A causal relationship between Mitofusin (MFN) 2 gene mutations and the hereditary axonal neuropathy Charcot-Marie-Tooth disease type 2A (CMT2A) was described over 15 years ago. During the intervening period much has been learned about MFN2 functioning in mitochondrial fusion, calcium signaling, and quality control, and the consequences of these MFN2 activities on cell metabolism, fitness, and development. Nevertheless, the challenge of defining the central underlying mechanism(s) linking mitochondrial abnormalities to progressive dying-back of peripheral arm and leg nerves in CMT2A is largely unmet. Here, a different perspective of why, in humans, MFN2 dysfunction preferentially impacts peripheral nerves is provided based on recent insights into its role in determining whether individual mitochondria will be fusion-competent and retained within the cell, or are fusion-impaired, sequestered, and eliminated by mitophagy. Evidence for and against a regulatory role of mitofusins in mitochondrial transport is reviewed, nagging questions defined, and implications on mitochondrial fusion, quality control, and neuronal degeneration discussed. Finally, in the context of recently described mitofusin activating peptides and small molecules, an overview is provided of potential therapeutic applications for pharmacological enhancement of mitochondrial fusion and motility in CMT2A and other neurodegenerative conditions.
Indexed as
Identifiers
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.