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Adam R. Wende
Researcher at University of Alabama at Birmingham
Publications - 101
Citations - 6488
Adam R. Wende is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Heart failure & Mitochondrion. The author has an hindex of 33, co-authored 85 publications receiving 5252 citations. Previous affiliations of Adam R. Wende include Sanford-Burnham Institute for Medical Research & University of Utah.
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Journal ArticleDOI
Diabetes-Related Cardiac Dysfunction
TL;DR: A review of mechanisms involving insulin resistance, dysregulation of microRNAs, and increased reactive oxygen species, as well as causes including both modifiable and non-modifiable risk factors, is published.
Journal ArticleDOI
Regulation of fatty acid metabolism by mTOR in adult murine hearts occurs independently of changes in PGC-1α
Yi Zhu,Jamie Soto,Brandon Anderson,Christian Riehle,Yi Cheng Zhang,Adam R. Wende,Deborah Jones,Donald A. McClain,E. Dale Abel +8 more
TL;DR: The role of rapamycin (mTOR) in the regulation of cardiac metabolism and mitochondrial respiration is not well established as discussed by the authors, but the role of mTOR in cardiac development, growth, and function is well established.
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My Sweetheart Is Broken: Role of Glucose in Diabetic Cardiomyopathy.
TL;DR: The unique contribution of glucose to heart disease and recent advances in defining mechanisms of action are discussed.
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Aberrant Water Homeostasis Detected by Stable Isotope Analysis
Shannon P. O'Grady,Adam R. Wende,Christopher H. Remien,Luciano O. Valenzuela,Lindsey E. Enright,Lesley A. Chesson,E. Dale Abel,Thure E. Cerling,James R. Ehleringer +8 more
TL;DR: It is demonstrated that untreated diabetes mellitus results in distinct combinations, or signatures, of the hydrogen and oxygen isotope ratios in body water, and shows that the δ2H and δ18O values of body water are correlated with increased water flux, suggesting altered blood osmolality, due to hyperglycemia, as the mechanism behind this correlation.
Journal ArticleDOI
GLUT1 deficiency in cardiomyocytes does not accelerate the transition from compensated hypertrophy to heart failure
Renata O. Pereira,Renata O. Pereira,Adam R. Wende,Curtis D. Olsen,Jamie Soto,Jamie Soto,Tenley A. Rawlings,Yi Zhu,Christian Riehle,Christian Riehle,E. Dale Abel,E. Dale Abel +11 more
TL;DR: GLUT1 deficiency in cardiomyocytes alters myocardial substrate utilization, but does not substantially exacerbate pressure-overload induced contractile dysfunction or accelerate the progression to heart failure.