ArticleExperimental and therapeutic medicine2018
MFN2 ameliorates cell apoptosis in a cellular model of Parkinson's disease induced by rotenone.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Charcot-Marie-Tooth type 2A variants of mitofusin 2 sensitize cells to apoptotic cell death.Journal of cell science · 2025Article
- MFN2-a multifaceted guardian against Parkinson's pathophysiology: mitochondria, ferroptosis, inflammation and oxidative stress.Frontiers in aging neuroscience · 2025Article
- Mitochondrial CaCell death & disease · 2021Article
- Using mitochondrial respiration inhibitors to design a novel model of bipolar disorder-like phenotype with construct, face and predictive validity.Translational psychiatry · 2021Article
- Friend or Foe: Lipid Droplets as Organelles for Protein and Lipid Storage in Cellular Stress Response, Aging and Disease.Molecules (Basel, Switzerland) · 2020Review
- A new target for an old DUB: UCH-L1 regulates mitofusin-2 levels, altering mitochondrial morphology, function and calcium uptake.Redox biology · 2020Article
- The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis.Oxidative medicine and cellular longevity · 2019Review
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Authors and funding
6 authors.
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Abstract
A number of studies indicated that apoptosis, a specific type of programmed cell death, contributed to the loss of dopaminergic neurons during progression of Parkinson's disease (PD). Previously, the authors of the present study demonstrated that apoptosis of dopaminergic neurons was mainly achieved via the mitochondria-mediated apoptosis pathway, however, the precise molecular mechanisms remain to be elucidated. The present study aimed to determine whether mitofusin-2 (MFN2), a mitochondrial protein, participated in the apoptosis of dopaminergic neurons in a cellular model of PD induced by rotenone. The present study demonstrated that the expression of MFN2 was relatively stable following treatment with rotenone. Lentiviral knockdown and overexpression experiments for the first time, to the best of the authors knowledge, revealed that MFN2 prevented rotenone-induced cell death by amelioration of apoptosis. These results revealed a protective role of MFN2 against apoptosis in an
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