Mitochondrial Energetics in the Heart in Obesity-Related Diabetes
By S. Boudina, S. Sena, H. Theobald, X. Sheng, Jordan J. Wright, Xia Hu, Salwa Aziz, Josie I. Johnson, H. Bugger, Vlad G. Zaha and 1 more. Diabetes, 2007
621 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/c113e20580fd4af3959d81953d5dcc79d4f46cf4
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cardiology and Cardiovascular Medicine
In Molecular Biology
In Physiology
Citations in the corpus
- Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, positive): “In this case, the protection was thought to be related to higher islet ATP or to the ATP = ADP ratio consequent on reduced UCP2.”
- Cardiac Metabolism and Its Interactions with Contraction, Growth, and Survival of the Cardiomyocte (2013, background): “Cardiac dysfunction in obesity and diabetes mellitus has been associated with increased myocardial oxygen consumption, reduced cardiac efficiency, and increased oxidative stress, suggesting that increased rates of FAO are detrimental to cardiac function (Figure 3).(102,105,106) As discussed above, o”
- Molecular mechanisms of diabetic cardiomyopathy (2014, neutral): “In animal models of diabetes, several independent groups reported increased mitochondrial protein tyrosine nitration, increased levels of lipid peroxidation products, decreased levels of reduced glutathione and induction of the antioxidant defence system [59, 75, 102, 103].”
- Cardiac remodeling in obesity. (2008, background): “We recently demonstrated that mitochondrial ROS production is increased in the hearts of db/db mice and is generated in complex I and possibly in complex III (31).”
- Mitochondrial dysfunction in pathophysiology of heart failure (2018, background): “Inhibition of ATP synthase activity not only impedes ATP production but also impairs electron flow and enhances ROS emission (128, 129).”
- Diabetic cardiomyopathy, causes and effects (2010, background): “Mitochondrial ROS generation or lipid peroxides such as hydroxynonenal have been shown to activate uncoupling proteins in heart muscle mitochondria [95] and were found to be increased in the hearts of db/db mice [32].”
- Glutathione Peroxidase-1 in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities (2011, neutral): “Although there are some studies to the contrary, decreased mitochondrial function and/or content are associated with insulin resistance in animal models as well as in human subjects (44, 171, 194, 365).”