ArticleActa myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology2022
Torin1 restores proliferation rate in Charcot-Marie-Tooth disease type 2A cells harbouring MFN2 (mitofusin 2) mutation.
Article in Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Myo-Inositol modulates AKT signalling, mitochondrial protein expression and intracellular Ca²⁺dynamics in human dermal fibroblasts.Scientific reports · 2026Article
- The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease.Biomolecules · 2025Review
- Autophagy and Senescence: The Molecular Mechanisms and Implications in Liver Diseases.International journal of molecular sciences · 2023Review
- Torin1 restores proliferation rate in Charcot-Marie-Tooth disease type 2A cells harbouring MFN2 (mitofusin 2) mutation.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2022Article
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Authors and funding
5 authors.
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Abstract
Objective: Mitofusin 2 (MFN2) is a mitochondrial outer membrane protein that serves primarily as a mitochondrial fusion protein but has additional functions including the tethering of mitochondrial-endoplasmic reticulum membranes, movement of mitochondria along axons, and control of the quality of mitochondria. Intriguingly, MFN2 has been referred to play a role in regulating cell proliferation in several cell types such that it acts as a tumour suppressor role in some forms of cancer. Previously, we found that fibroblasts derived from a Charcot-Marie-Tooth disease type 2A (CMT2A) patient with a mutation in the GTPase domain of MFN2 exhibit increased proliferation and decreased autophagy. Methods: Primary fibroblasts from a young patient affected by CMT2A harbouring c.650G > T/p.Cys217Phe mutation in the Results: Herein, we demonstrated that the mammalian target of rapamycin complex 2 (mTORC2) is highly activated in the CMT2A Conclusions: Overall, our study provides evidence for mTORC2, as a novel molecular target that lies upstream of AKT to restore the cell proliferation rate in CMT2A fibroblasts.
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