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Faculty Detail    
Name ADAM R WENDE
Associate Professor		  
Campus Address BMR2 506 Zip 2186
Phone  (205) 975-6272
E-mail  adamwende@uabmc.edu
Other websites PubMed
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Lab Website
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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  Joint 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  Ctr for Clinical & Translational Sci  Ctr for Clinical & Translational Sci Associate Professor
Center  Ctr for Exercise Medicine (Org Ret)  Ctr for Exercise Medicine (Org Ret) Associate Professor
Center  Minority Health & Research Center  Minority Health & Research Center Associate Professor
Center  Nutrition Sciences Research  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 and Fellow (FCVS)  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 79 in print or press.  N/A 
Pepin ME, Ha CM, Potter LA, Bakshi S, Barchue JP, Haj asaad A, Pogwizd SM, Pamboukian SV, Hidalgo BA, Vickers SM and Wende AR#. Racial and socioeconomic disparity associates with differences in cardiac DNA methylation among men with end-stage heart failure. American Journal of Physiology – Heart and Circulatory Physiology, 320(5):H2066-H2079, 2021. (COVER ARTICLE)

Most recent addition to our work in DNA methylation mediated changes in cardiac gene expression with a special focus on racial differences in the severity of heart failure and how socioeconomic disparities are associated with them. 		 33769919 
Chatham JC, Zhang J and Wende AR. Role of O-linked N-acetylglucosamine protein modification in cellular (patho)physiology. Physiological Reviews, 101(2):427-493, 2021.

Comprehensive review on protein O-GlcNAcylation highlighting several unanswered questions. 		 32730113 
Lopaschuk GD, Karwi QG, Tian R, Wende AR and Abel ED. Cardiac energy metabolism in heart failure. Circulation Research, 128(10):1487-1513, 2021.

Comprehensive review on cardiac energy metabolism with recent updates. 		 33983836 
Brahma MK, Ha CM, Pepin ME, Mia S, Sun Z, Chatham JC, Habegger KM, Abel ED, Paterson ED, Young ME and Wende AR. Increased glucose availability attenuates myocardial ketone body utilization. Journal of the American Heart Association, 9(15):e013039, 2020.

Seminal work from my first postdoc Dr. Brahma (AHA funded). This study rediscovers the impact of ketone body metabolism with a focus on its regulation by diabetes, glucose, and protein O-GlcNAcylation. 		 32750298 
Wende AR, Schell JC, Ha CM, Pepin ME, Khalimonchuk O, Schwertz H, Pereira RO, Brahma MK, Tuinei J, Contreras-Ferrat A, Wang L, Andrizzi CA, Olsen CD, Bradley WE, Dell’Italia JL, Dillmann WH, Litwin SE and Abel ED. Maintaining myocardial glucose utilization in diabetic cardiomyopathy accelerates mitochondrial and contractile dysfunction. Diabetes, 69(10):2094-2111, 2020. (SEE COMMENTARY SAME ISSUE PMID: 32958606)

Summary paper of the primary hypothesis of my postdoctoral work (K99R00) with additions from my independent laboratory (R01). 		 32366681 
Wende AR. Post-translational modifications of the cardiac proteome in diabetes and heart failure. Proteomics Clinical Applications, 10(1):25-38, 2016. (COVER ARTICLE)

First independent review highlighting several of the mechanisms we are interested in studying in the development of heart failure, special focus on protein O-GlcNAcylation and acetylation. 		 26140508 
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)

First fully independent study from our laboratory defining the role of DNA methylation in heart failure gene expression reprogramming, focused on ischemic heart failure. Seminal publication from my first graduate (MSTP) student Dr. Pepin (NIH F30 funded). 		 30089854 
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.

Second half of my thesis work defining the functional role of exercise induced skeletal muscle PGC-1alpha in the regulation of glycogen replenishment via PDK4. 		 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.

Key chapter of my thesis work defining the transcriptional regulation of PDK4 via PGC-1alpha mediated co-activation of ERRalpha. 		 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.

My first and most cited publication. Collaboration during my thesis work with Drs. Baar and Holloszy showing skeletal muscle PGC-1alpha induction following exercise.  		 12468452 
 

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