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Faculty Detail    
Name ADAM R WENDE
Associate Professor		  
Campus Address BMR2 506 Zip 2186
Phone  (20-5) -272
E-mail  adamwende@uabmc.edu
Other websites PubMed
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ResearchGate
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Education
Undergraduate  Knox College    2000  BA in Biochemistry and Biology 
Graduate  Washington University in St. Louis    2006  PhD in Molecular Cellular Biology 
Fellowship  University of Utah    2013  Postdoctoral studies 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Associate Professor
Secondary  Biomedical Engineering  Biomedical Engineering Assistant Professor
Center  Center for AIDS Research  Center for AIDS Research Associate Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Associate Professor
Center  Comprehensive Cardiovascular Ctr  Comprehensive Cardiovascular Ctr Associate Professor
Center  Comprehensive Diabetes Center  Comprehensive Diabetes Center Associate Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Associate Professor
Center  Cell, Developmntl, & Integrative Biology  Ctr for Exercise Medicine Associate Professor
Center  General Clinical Research Center  Minority Health & Research Center Associate Professor
Center  Nutrition Sciences   Nutrition Obesity Res Ctr (NORC) Associate Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 
Cell, Molecular, & Developmental Biology 
Genetics, Genomics and Bioinformatics 
Molecular and Cellular Pathology Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Since 2000, Dr. Wende has explored the regulation of metabolism and mitochondrial function with a specific focus on glucose utilization in heart and muscle. After completing his undergraduate biochemistry degree and an Honors Thesis with Dr. Mark R. Brodl at Knox College in Galesburg, IL he went on to undertake his Ph.D. training in the Cardiology Department as part of the Division of Biology and Biomedical Sciences at Washington University in St. Louis, MO studying transcriptional regulation with Dr. Daniel P. Kelly. After completing his thesis work in the spring of 2006, he joined the University of Utah to pursue his postdoctoral studies with Dr. E. Dale Abel examining upstream regulation by cellular signaling and the resulting changes in mitochondrial physiology. Then in August of 2013, he joined the faculty at The University of Alabama at Birmingham in the Division of Molecular and Cellular Pathology as an Assistant Professor. His work has been funded by the American Heart Association, the JDRF, and most recently by an NIH R01 award. With these training experiences he has expanded his independent research program through use of transgenic and diabetes mouse models to identify molecular and genetic mechanisms of glucose-mediated control of mitochondrial function. His outside interests include time with his wife and two daughters and running marathons.

Society Memberships
Organization Name Position Held Org Link
American Diabetes Association  Member  ADA 
American Heart Association  Member and Fellow (FAHA)  AHA 
American Physiological Society  Member  APS 
American Society for Biochemistry and Molecular Biology  Member  ASBMB 
 



Research/Clinical Interest
Title
Glucose-mediated remodeling of cardiac DNA methylation
Description
Specifically, work in the laboratory has two primary goals: 1) to determine the role of metabolic substrate switching in the hearts of individuals with diabetes or heart failure, and 2) to define the role of cellular glucose delivery on post-translational regulation of mitochondrial enzyme activity and epigenetic regulation of gene expression that together may lead to the development of diabetic cardiomyopathy. The primary goal of the R01-funded research is to determine the role glucose fluctuations in the regulation of DNA methylation in transgenic models of glucose uptake and diabetes models. Other projects in the laboratory include determining the role of the protein post-translational modification O-GlcNAc in regulating cardiac cellular function and define the role that changes in glucose levels have on long-lasting epigenetic regulation of gene expression in a process termed “glycemic memory”. Recent studies include work defining these molecular pathways in human heart failure biopsies to determine etiology specific epigenetic signatures (as published here: https://www.nature.com/articles/s41374-018-0104-x). Finally, we have initial work looking at human samples to define racial differences in epigenetic changes that in turn impact susceptibility to diabetes and heart failure. By determining these molecular signatures of altered protein regulation and DNA structure/regulation we aim to provide critical knowledge to determining future therapeutic interventions for diabetic and heart failure patients.

Selected Publications 
Publication PUBMEDID
Please use PubMed link under "Other websites" above for full list of published manuscripts. Here is a selection of the most relevant 10 of 58 in print or press.  N/A 
Pepin ME, Ha CM, Crossman DK, Litovsky SH, Varambally S, Barchue JP, Pamboukian SV, Diakos NA, Drakos SG, Pogwizd SM and Wende AR. Genome-wide DNA methylation changes associated with cardiac transcriptional profiles in human ischemic heart failure. Laboratory Investigation, 99(3):371-386, 2019. (COVER ARTICLE)  30089854 
Koentges C*, Pepin ME*, Müsse C, Pfeil K, Viteri Alvarez SV, Hoppe N, Hoffmann MM, Odening KE, Sossalla S, Zirlik A, Hein L, Bode C, Wende AR# and Bugger H#. Gene expression analysis to identify mechanisms underlying heart failure susceptibility in mice and humans. Basic Research in Cardiology, 113(1):1-17, 2018.  29288409 
Wende AR, Kim J, Holland W, Wayment BE, O'Neill BT, Tuinei J, Brahma MK, Pepin ME, McCrory MA, Luptak I, Halade GV, Litwin SE, Abel ED. Glucose transporter 4 (GLUT4) deficient hearts develop maladaptive hypertrophy in response to physiologic or pathologic stresses. American Journal of Physiology. Heart and Circulatory Physiology, 313(6):H1098-H1108, 2017.  28822962 
Wende AR. Post-translational modifications of the cardiac proteome in diabetes and heart failure. Proteomics Clinical Applications, 10(1):25-38, 2016.  26140508 
Wende AR, Brahma MK, McGinnis GR and Martin ME. Metabolic origins of heart failure. Journal of the American College of Cardiology, 2(3):297-310, 2017.  28944310 
Wende AR*, O’Neill BT*, Bugger H, Riehle C, Tuinei J, Buchanan J, Tsushima K, Wang L, Caro P, Guo A, Sloan C, Kim BJ, Wang X, Pereira RO, McCrory MA, Nye BG, Benavides GA, Darley-Usmar VM, Shioi T, Weimer B and Abel ED. Enhanced cardiac Akt/protein kinase B signaling contributes to pathological cardiac hypertrophy in part by impairing mitochondrial function via transcriptional repression of mitochondrion-targeted nuclear genes. Molecular and Cellular Biology, 35(5):831-846, 2015.  25535334 
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, Sheng X, Weimer BC, Gottlieb RA, White MF and Abel ED. Insulin receptor substrates are required for suppressing neonatal autophagy in the heart. The Journal of Clinical Investigation, 123(12):5319-5333, 2013.  24177427 
Wende AR, Schaeffer PJ, Parker GL, Zechner C, Han DH, Chen MM, Hancock CR, Lehman JJ, Huss JH, McClain DA, Holloszy JO and Kelly DP. A role for the transcriptional coactivator PGC-1alpha in muscle refueling. The Journal of Biological Chemistry, 282(50):36642-36651, 2007.  17932032 
Wende AR, Huss JM, Schaeffer PJ, Giguère V and Kelly DP. PGC-1alpha coactivates PDK4 gene expression via the orphan nuclear receptor ERRalpha: A mechanism for transcriptional control of muscle glucose metabolism. Molecular and Cellular Biology, 25(24):10684-10694, 2005.  16314495 
Baar K, Wende AR, Jones TE, Marison M, Nolte LA, Chen M, Kelly DP and Holloszy JO. Adaptations of muscle to exercise: rapid increase in the transcriptional coactivator PGC-1. The FASEB Journal, 16(14):1879-1886, 2002. (CITED >1,000 TIMES)  12468452 
 

Keywords
Diabetes, Hypertension, Exercise, Mitochondria, Metabolism, Glucose, Epigenetics, Gene expression, transcription, O-GlcNAc, protein modifications, DNA methylation, Histone modification, GLUT4, PDK2, PDK4