• 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.
  • Selected Publications

    Academic Article

    Year Title Altmetric
    2022 Vitamin A preserves cardiac energetic gene expression in a murine model of diet-induced obesity 2022
    2022 Guidelines on models of diabetic heart disease 2022
    2022 CrossTalk opposing view: Ketone bodies are not an important metabolic fuel for the heart 2022
    2022 Rebuttal from Manoja K. Brahma, Adam R. Wende and Kyle S. McCommis 2022
    2022 Cardiomyocyte stromal interaction molecule 1 is a key regulator of Ca2+-dependent kinase and phosphatase activity in the mouse heartPhysiological Reports.  10. 2022
    2021 The Identification of a Novel Calcium-Dependent Link Between NAD+ and Glucose Deprivation-Induced Increases in Protein O-GlcNAcylation and ER StressFrontiers in Molecular Biosciences.  8. 2021
    2021 Identification of Nrf2-responsive microRNA networks as putative mediators of myocardial reductive stressScientific Reports.  11. 2021
    2021 Heart Failure in Pulmonary Arterial Hypertension Is Just a WNK1 AwayJACC: Basic to Translational Science.  6:851-853. 2021
    2021 Normalizing glucose levels reconfigures the mammary tumor immune and metabolic microenvironment and decreases metastatic seedingCancer Letters.  517:24-34. 2021
    2021 FGF21-FGFR4 signaling in cardiac myocytes promotes concentric cardiac hypertrophy in mouse models of diabetes 2021
    2021 Pyruvate dehydrogenase kinase 1 and 2 deficiency reduces high-fat diet-induced hypertrophic obesity and inhibits the differentiation of preadipocytes into mature adipocytesExperimental and Molecular Medicine.  53:1390-1401. 2021
    2021 Branched chain amino acids selectively promote cardiac growth at the end of the awake periodJournal of Molecular and Cellular Cardiology.  157:31-44. 2021
    2021 Cardiac Energy Metabolism in Heart FailureCirculation Research.  128:1487-1513. 2021
    2021 Racial and socioeconomic disparity associates with differences in cardiac DNA methylation among men with end-stage heart failure 2021
    2021 Role of o-linked n-acetylglucosamine proteinmodification in cellular (Patho) physiologyPhysiological Reviews.  101:427-493. 2021
    2021 The human aortic endothelium undergoes dose-dependent DNA methylation in response to transient hyperglycemiaExperimental Cell Research.  400. 2021
    2020 Maintaining myocardial glucose utilization in diabetic cardiomyopathy accelerates mitochondrial dysfunctionDiabetes.  69:2094-2111. 2020
    2020 Differential DNA Methylation Encodes Proliferation and Senescence Programs in Human Adipose-Derived Mesenchymal Stem CellsFrontiers in Genetics.  11. 2020
    2020 Insulin receptor substrates differentially exacerbate insulin-mediated left ventricular remodelingJCI Insight.  5. 2020
    2020 The SETD6 Methyltransferase Plays an Essential Role in Hippocampus-Dependent Memory FormationBiological Psychiatry.  87:577-587. 2020
    2020 MitoQ regulates redox-related noncoding RNAs to preserve mitochondrial network integrity in pressure-overload heart failure 2020
    2020 Increased glucose availability attenuates myocardial ketone body utilizationJournal of the American Heart Association.  9. 2020
    2019 Dysregulation of the Mitochondrial Proteome Occurs in Mice Lacking Adiponectin Receptor 1Frontiers in Endocrinology.  10. 2019
    2019 Novel role of the ER/SR Ca2+ sensor STIM1 in the regulation of cardiac metabolism 2019
    2019 Epigenetics in the development of diabetic cardiomyopathyEpigenomics.  11:469-472. 2019
    2019 Genome-wide DNA methylation encodes cardiac transcriptional reprogramming in human ischemic heart failureLaboratory Investigation.  99:371-386. 2019
    2019 Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in miceRedox Biology.  21. 2019
    2019 The Growing Case for Use of SGLT2i in Heart Failure: Additional Benefits of Empagliflozin in a HFpEF Rodent ModelJACC: Basic to Translational Science.  4:38-40. 2019
    2019 Resident macrophages reprogram toward a developmental state after acute kidney injuryJCI Insight.  4. 2019
    2019 DNA methylation reprograms cardiac metabolic gene expression in end-stage human heart failure 2019
    2019 Prolactin receptor signaling regulates a pregnancy-specific transcriptional program in mouse islets 2019
    2018 Glucagon receptor signaling regulates energy metabolism via hepatic farnesoid X receptor and fibroblast growth factor 21Diabetes.  67:1773-1782. 2018
    2018 Antiretroviral therapy potentiates high-fat diet induced obesity and glucose intoleranceMolecular Metabolism.  12:48-61. 2018
    2018 Temporal partitioning of adaptive responses of the murine heart to fastingLife Sciences.  197:30-39. 2018
    2018 Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induce Post-Translational Modifications of AKAP121, DRP1, and OPA1 That Promote Mitochondrial FissionCirculation Research.  122:58-73. 2018
    2018 Gene expression analysis to identify mechanisms underlying heart failure susceptibility in mice and humansBasic Research in Cardiology.  113. 2018
    2017 Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in response to physiological or pathological stresses 2017
    2017 Genetic disruption of the cardiomyocyte circadian clock differentially influences insulin-mediated processes in the heartJournal of Molecular and Cellular Cardiology.  110:80-95. 2017
    2017 Diabetes-related cardiac dysfunctionEndocrinology and Metabolism.  32:171-179. 2017
    2017 Metabolic Origins of Heart FailureJACC: Basic to Translational Science.  2:297-310. 2017
    2017 O-GlcNAcylation and cardiovascular diseaseBiochemical Society Transactions.  45:545-553. 2017
    2017 My sweetheart is broken: Role of glucose in diabetic cardiomyopathy 2017
    2016 Redox biology and the interface between bioenergetics, autophagy and circadian control of metabolismFree Radical Biology and Medicine.  100:94-107. 2016
    2016 Post-translational modifications of the cardiac proteome in diabetes and heart failure 2016
    2015 Phosphoinositide dependent protein kinase 1 is required for exercise-induced cardiac hypertrophy but not the associated mitochondrial adaptationsJournal of Molecular and Cellular Cardiology.  89:297-305. 2015
    2015 Unsticking the broken diabetic heart: O-GlcNAcylation and calcium sensitivityDiabetes.  64:3339-3341. 2015
    2015 Myocardial mitochondrial dysfunction in mice lacking adiponectin receptor 1Basic Research in Cardiology.  110. 2015
    2015 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 genesMolecular and Cellular Biology.  35:831-846. 2015
    2014 Cardiomyocyte-specific BMAL1 plays critical roles in metabolism, signaling, and maintenance of contractile function of the heartJournal of Biological Rhythms.  29:257-276. 2014
    2014 Intramuscular fat and inflammation differ in older adults: The impact of frailty and inactivityJournal of Nutrition, Health and Aging.  18:532-538. 2014
    2014 The absence of insulin signaling in the heart induces changes in potassium channel expression and ventricular repolarization 2014
    2014 GLUT1 deficiency in cardiomyocytes does not accelerate the transition from compensated hypertrophy to heart failureJournal of Molecular and Cellular Cardiology.  72:95-103. 2014
    2014 Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise trainingMolecular and Cellular Biology.  34:3450-3460. 2014
    2014 Intramuscular fat and inflammation differ in older adults: The impact of frailty and inactivityJournal of Nutrition, Health and Aging.  18:532-538. 2014
    2014 Maintaining PGC-1α expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function 2014
    2013 Insulin receptor substrate signaling suppresses neonatal autophagy in the heartJournal of Clinical Investigation.  123:5319-5333. 2013
    2013 APpEaLINg therapeutic target for obesity cardiomyopathy?Journal of Molecular and Cellular Cardiology.  63:165-168. 2013
    2013 Regulation of fatty acid metabolism by mTOR in adult murine hearts occurs independently of changes in PGC-1α 2013
    2013 Metabolic Determinants of Electrical Failure in Ex-Vivo Canine Model of Cardiac Arrest: Evidence for the Protective Role of Inorganic PyrophosphatePLoS One.  8. 2013
    2013 Regionalmuscle glucose uptake remains elevated one week after cessation of resistance training independent of altered insulin sensitivity response in older adults with type 2 diabetesJournal of Endocrinological Investigation.  36:111-117. 2013
    2013 Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation 2013
    2013 Absence of glucose transporter 4 diminishes electrical activity of mouse hearts during hypoxiaExperimental Physiology.  98:746-757. 2013
    2013 Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunctionJournal of the American Heart Association.  2. 2013
    2012 Mechanisms of lipotoxicity in the cardiovascular systemCurrent Hypertension Reports.  14:517-531. 2012
    2012 Genetic loss of insulin receptors worsens cardiac efficiency in diabetesJournal of Molecular and Cellular Cardiology.  52:1019-1026. 2012
    2012 Cytosolic, but not mitochondrial, oxidative stress is a likely contributor to cardiac hypertrophy resulting from cardiac specific GLUT4 deletion in mice 2012
    2011 The maximal downstroke of epicardial potentials as an index of electrical activity in mouse heartsIEEE Transactions on Biomedical Engineering.  58:3175-3183. 2011
    2011 PGC-1β deficiency accelerates the transition to heart failure in pressure overload hypertrophyCirculation Research.  109:783-793. 2011
    2011 Expression of slow skeletal TnI in adult mouse hearts confers metabolic protection to ischemiaJournal of Molecular and Cellular Cardiology.  51:236-243. 2011
    2011 Knockout of insulin receptors in cardiomyocytes attenuates coronary arterial dysfunction induced by pressure overload 2011
    2010 Aberrant water homeostasis detected by stable isotope analysisPLoS One.  5. 2010
    2010 Loss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic akita mice 2010
    2010 Preferential oxidation of triacylglyceride-derived fatty acids in heart is augmented by the nuclear receptor PPARαCirculation Research.  107:233-241. 2010
    2010 Lipotoxicity in the heart 2010
    2008 Insulin-like growth factor I receptor signaling is required for exercise-induced cardiac hypertrophy 2008
    2007 A role for the transcriptional coactivator PGC-1α in muscle refuelingJournal of Biological Chemistry.  282:36642-36651. 2007
    2007 Cardiac hypertrophy caused by peroxisome proliferator-activated receptor-γ agonist treatment occurs independently of changes in myocardial insulin signaling 2007
    2007 A Conserved Role for Phosphatidylinositol 3-Kinase but Not Akt Signaling in Mitochondrial Adaptations that Accompany Physiological Cardiac HypertrophyCell Metabolism.  6:294-306. 2007
    2006 Diminished hepatic gluconeogenesis via defects in tricarboxylic acid cycle flux in peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)-deficient miceJournal of Biological Chemistry.  281:19000-19008. 2006
    2005 PGC-1α coactivates PDK4 gene expression via the orphan nuclear receptor ERRα: A mechanism for transcriptional control of muscle glucose metabolismMolecular and Cellular Biology.  25:10684-10694. 2005
    2005 PGC-1α deficiency causes multi-system energy metabolic derangements: Muscle dysfunction, abnormal weight control and hepatic steatosisPLoS Biology.  3:0672-0687. 2005
    2004 Calcineurin and calcium/calmodulin-dependent protein kinase activate distinct metabolic gene regulatory programs in cardiac muscleJournal of Biological Chemistry.  279:39593-39603. 2004
    2002 Adaptations of skeletal muscle to exercise: Rapid increase in the transcriptional coactivator PGC-1 2002

    Research Overview

  • Glucose-mediated remodeling of cardiac DNA methylation - 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.

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

  • Doctor of Philosophy in Cell / Cellular and Molecular Biology, Washington University/St. Louis 2006
  • Full Name

  • Adam Wende