Adam Wende

Personal Information
Title Assistant Professor
Expertise Cardiomyopathy
Institution University of Alabama at Birmingham
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Data Summary
Grants/SubContracts 1
Progress Reports 1
Publications 10
Protocols 0
Committees 2

Human DNA Methylation Signatures to Define Diabetic Cardiac Subtypes
Cardiovascular diseases remain the major cause of death in patients with diabetes. Determining the role of diabetes in the progression of heart disease is critical to the development of personalized medicine. Heart failure is accompanied by a reprogramming of gene expression, a process that is not completely understood. Recently, epigenetics or the contribution of non-coding RNAs, post-translational modifications of histone proteins, and/or methylation of DNA has emerged as a component of transcriptional regulation. Each of these pathways directly impacts gene regulation in development, cancer, mental illness, heart failure, and diabetes. Defining the contribution of each mode of regulation is a hurdle to developing effective interventions. Studies in both animal models and humans have now shown that DNA methylation is regulated both transgenerationally and acutely. Specifically, parental diet can modify DNA methylation patterns of offspring. This process can be reproduced acutely in cell culture by treating cells with high glucose. The contribution of glucose fluctuations in patients with either Type 1 or Type 2 diabetes mellitus has been linked to the development of diabetic complications. This process is termed “metabolic memory” and is associated with epigenetic changes. Despite the growing wealth of knowledge on epigenetics, diabetes, and the subsequent physiological changes, relatively little is known about their role on myocardial tissue. The hypothesis to be tested in the current study is that cardiac DNA methylation distinguishes unique pathways in the development of heart failure. A critical barrier to defining tissue specific molecular pathways in the regulation of gene expression is access to human heart samples. This study will interrogate changes in DNA modifications in the combination of diabetic, non-diabetic, heart failure, and non-heart failure human cardiac tissue. The aim of this study is to define DNA methylation signatures that will distinguish diabetic cardiomyopathy and heart failure. The year of pilot and feasibility funding will provide the means to identify potential genetic changes that will then be tested for direct functional impact on gene expression in future R01 grant applications.

Progress Reports

Annual Reports
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Year: 2018; Items: 1

Genome-wide DNA methylation encodes cardiac transcriptional reprogramming in human ischemic heart failure.
Pepin ME, Ha CM, Crossman DK, Litovsky SH, Varambally S, Barchue JP, Pamboukian SV, Diakos NA, Drakos SG, Pogwizd SM, Wende AR
Laboratory investigation; a journal of technical methods and pathology, 2018

Year: 2015; Items: 1


Year: 2014; Items: 3

The absence of insulin signaling in the heart induces changes in potassium channel expression and ventricular repolarization.
Lopez-Izquierdo A, Pereira RO, Wende AR, Punske BB, Abel ED, Tristani-Firouzi M
American journal of physiology. Heart and circulatory physiology, 2014 (306), H747 - H754
Submitted Externally
Maintaining PGC-1a expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function.
Pereira RO, Wende AR, Crum A, Hunter D, Olsen CD, Rawlings T, Riehle C, Ward WF, Abel ED
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014 (28), 3691 - 702
Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise training.
Riehle C, Wende AR, Zhu Y, Oliveira KJ, Pereira RO, Jaishy BP, Bevins J, Valdez S, Noh J, Kim BJ, Moreira AB, Weatherford ET, Manivel R, Rawlings TA, Rech M, White MF, Abel ED
Molecular and cellular biology, 2014 (34), 3450 - 60

Year: 2013; Items: 2

Absence of glucose transporter 4 diminishes electrical activity of mouse hearts during hypoxia.
Sohn K, Wende AR, Abel ED, Moreno AP, Sachse FB, Punske BB
Experimental physiology, 2013 (98), 746 - 757
Submitted Externally
Insulin receptor substrate signaling suppresses neonatal autophagy in the heart.
Riehle C, Wende AR, Sena S, Pires KM, Pereira RO, Zhu Y, Bugger H, Frank D, Bevins J, Chen D, Perry CN, Dong XC, Valdez S, Rech M, Sheng X, Weimer BC, Gottlieb RA, White MF, Abel ED
The Journal of clinical investigation, 2013 (123), 5319 - 5333

Year: 2012; Items: 1

Cytosolic, but not mitochondrial, oxidative stress is a likely contributor to cardiac hypertrophy resulting from cardiac specific GLUT4 deletion in mice.
Li Y, Wende AR, Nunthakungwan O, Huang Y, Hu E, Jin H, Boudina S, Abel ED, Jalili T
The FEBS journal, 2012 (279), 599 - 611
Submitted Externally

Year: 2010; Items: 1

Aberrant water homeostasis detected by stable isotope analysis.
O'Grady SP, Wende AR, Remien CH, Valenzuela LO, Enright LE, Chesson LA, Abel ED, Cerling TE, Ehleringer JR
PLoS ONE, 2010 (5), e11699
Submitted Externally

Year: 2007; Items: 1

A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy.
O'Neill BT, Kim J, Wende AR, Theobald HA, Tuinei J, Buchanan J, Guo A, Zaha VG, Davis DK, Schell JC, Boudina S, Wayment B, Litwin SE, Shioi T, Izumo S, Birnbaum MJ, Abel ED
Cell Metabolism, 2007 (6), 294 - 306
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