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Adam R. Wende, PhD, FAHA

Adam R. Wende, Ph.D. Associate Professor
Department of Molecular and Cellular Pathology
BMR2 Rm 506
Phone: (205) 975-6272
Web Site

Dr. Wende has been exploring the regulation of glucose utilization in heart and muscle since 2000. After completing his undergraduate biochemistry degree at Knox College in Galesburg, IL with Dr. Mark Brodl, he went on to undertake his PhD training in the Cardiology Department at Washington University in St. Louis, MO studying transcriptional regulation (via PGC-1alpha) with Dr. Daniel P. Kelly. He then joined the University of Utah in 2006 to pursue his postdoctoral studies with Dr. E. Dale Abel examining upstream regulation by cellular signaling (Akt, PI3K, etc.) 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.

His work has been funded by the American Heart Association, the JDRF, an NIH K99, and more recently as PI and Co-I on various NIH R01 awards. With the listed training experiences, he has expanded his research through use of transgenic and diabetes mouse models to identify molecular and genetic mechanisms of glucose-mediated control of mitochondrial function. The laboratories recent focus has taken these observations into studies of the human heart as published here (PMID: 30089854 and 31298559) and described below. His outside interests include time with his wife and two daughters as well as running marathons.

Research Description

Mechanisms of glucose mediated regulation of cardiac mitochondrial function- 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 R00 funded research is to determine the role the protein post-translational modification O-GlcNAc has 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”. By defining 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.