Increased production of reactive oxygen species in hyperglycemic conditions requires dynamic change of mitochondrial morphology.
By Tianzheng Yu, J. Robotham, Y. Yoon. Proceedings of the National Academy of Sciences of the United States of America, 2006
1,220 citations recorded by the source corpus.
Subfields: Molecular Biology, Pathology and Forensic Medicine, Physiology
View Paper: https://www.semanticscholar.org/paper/45c22182b68c57318be90cd987269669833f5d66
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Citations in the corpus
- The Interplay Between Mitochondrial Dynamics and Mitophagy (2011, background): “On the other hand, excessive and unbalanced fission under a variety of metabolic insults has deleterious effects in a variety of tissues: Cardiac and skeletal myocytes Knockdown of Drp1 reduces significantly hyperglycemiainduced apoptosis in H2c9 (124) and HL-1 cardiac cells (125) and prevents ROS f”
- Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “Extended exposure to high-glucose conditions provoked a periodic and prolonged increase in ROS production, which could be prevented by inhibition of mitochondrial fission [63].”
- Nitric oxide‐induced mitochondrial fission is regulated by dynamin‐related GTPases in neurons (2006, background): “It has been suggested that dynamin-related GTPases may have additional functions including regulation of bioenergetics and ion homeo- stasis (Pich et al, 2005; Yu et al, 2006).”