Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis
By David Sebastián, M. Hernández-Alvarez, J. Segalés, E. Sorianello, J. Muñoz, D. Sala, A. Waget, M. Liesa, J. C. Paz, Peddinti V. Gopalacharyulu and 5 more. Proceedings of the National Academy of Sciences of the United States of America, 2012
662 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/4992430165848c2f2d9bc0870a9dee6cb991b7f4
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Citations in the corpus
- Insulin resistance: Review of the underlying molecular mechanisms (2018, background): “Oxidative stress plays a prominent role in IR and mitochondria are a major source of free radicals (Rains & Jain, 2011; Sebastian et al., 2012).”
- Pathophysiology of Type 2 Diabetes Mellitus (2020, background): “Deregulation of mitochondria dynamics with a shift towards fission promotes metabolic dysfunction as demonstrated by the onset of obesity and IR following the ablation of fusion protein in mice [141,142].”
- Inflammation, Defective Insulin Signaling, and Mitochondrial Dysfunction as Common Molecular Denominators Connecting Type 2 Diabetes to Alzheimer Disease (2014, background): “Interestingly, mitochondrial dysfunction and increased ROS generation were recently found to activate JNK and to lead to insulin resistance in skeletal muscle and liver (133).”
- Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure (2013, background): “This is in part due to an additional site for superoxide formation (ETF-Qo, an exclusive site for electron entry into the ETC through fatty acid beta oxidation) (Seifert et al., 2010).”
- Endocrine disrupting chemicals: exposure, effects on human health, mechanism of action, models for testing and strategies for prevention (2019, background): “Changes in mitochondrial fission and fusion contribute to mitochondrial dysfunction, oxidative stress and β-cell apoptosis that may cause disrupted glucose homeostasis [139, 154].”