ArticleMolecular biology reports2014
Mitofusin 2 deficiency leads to oxidative stress that contributes to insulin resistance in rat skeletal muscle cells.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Major Royal Jelly Proteins promote C2C12 myotubes differentiation by improving mitochondrial function.Frontiers in nutrition · 2025Article
- Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds.Current nutrition reports · 2024Review
- MFN2 deficiency affects calcium homeostasis in lung adenocarcinoma cells via downregulation of UCP4.FEBS open bio · 2023Article
- Article
- ACTA1 H40Y mutant iPSC-derived skeletal myocytes display mitochondrial defects in an in vitro model of nemaline myopathy.Experimental cell research · 2023Article
- The role of CD36-Fabp4-PPARγ in skeletal muscle involves insulin resistance in intrauterine growth retardation mice with catch-up growth.BMC endocrine disorders · 2022Article
- Mitochondrial Dynamics and Mitochondria-Lysosome Contacts in Neurogenetic Diseases.Frontiers in neuroscience · 2022Article
- Ketone Ester D-β-Hydroxybutyrate-(R)-1,3 Butanediol Prevents Decline in Cardiac Function in Type 2 Diabetic Mice.Journal of the American Heart Association · 2021Article
- Reduced electron transport chain complex I protein abundance and function in Mfn2-deficient myogenic progenitors lead to oxidative stress and mitochondria swelling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- RNA binding protein HuD contributes to β-cell dysfunction by impairing mitochondria dynamics.Cell death and differentiation · 2020Article
- In vivo real-time dynamics of ATP and ROS production in axonal mitochondria show decoupling in mouse models of peripheral neuropathies.Acta neuropathologica communications · 2019Article
- Shexiang Baoxin Pill Alleviates the Atherosclerotic Lesions in Mice via Improving Inflammation Response and Inhibiting Lipid Accumulation in the Arterial Wall.Mediators of inflammation · 2019Article
- Ipragliflozin improves mitochondrial abnormalities in renal tubules induced by a high-fat diet.Journal of diabetes investigation · 2018Article
- NEFA-induced ROS impaired insulin signalling through the JNK and p38MAPK pathways in non-alcoholic steatohepatitis.Journal of cellular and molecular medicine · 2018Article
- The p75BMC research notes · 2017Article
- Glucose-regulated protein 75 determines ER-mitochondrial coupling and sensitivity to oxidative stress in neuronal cells.Cell death discovery · 2017Article
- Mitofusin 2 ablation increases endoplasmic reticulum-mitochondria coupling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitofusin 2 (Mfn2) is a dynamin-like protein anchored in the outer mitochondrial membrane that plays a crucial role in ensuring optimal mitochondrial morphological homeostasis. It has been shown that reduced expression of Mfn2 is associated with insulin resistance, but the mechanism is still unclear. We investigated whether Mfn2 deficiency leads to impaired insulin sensitivity via elevated oxidative stress. L6 skeletal muscle cells were treated with palmitate and Mfn2 expression was repressed by transfection with antisense Mfn2. Levels of antioxidant enzymes, reactive oxygen species (ROS), the phosphorylation of c-Jun N-terminal Kinase (JNK) and nuclear factor-κB (NF-κB) and the mitochondrial membrane potential (Δψm) were measured. The results showed palmitate-induced insulin resistance of skeletal muscle cells was accompanied by Mfn2 repression. Meanwhile, the cells had decreased Δψm and activity of antioxidant enzymes which could increase production of ROS, phosphorylation of JNK and NF-κB. When Mfn2 was up-regulated in palmitate-treated cells, oxidative stress and insulin resistance was alleviated. Furthermore, knock-down of Mfn2 in control cells enhanced oxidative stress. Mfn2 deficiency led to increased superoxide concentration and activation of JNK as well as NF-κB associated with insulin signaling. In conclusion, Mfn2 is a potent repressor for oxidative stress and regulation of Mfn2 expression may prove to be a potential method to circumvent insulin resistance.
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