Justin L. Grobe, PhD, FAHA, FAPS

Dr. Grobe completed undergraduate training in Biology and Chemistry at Hope College (Holland, MI), and worked in the research laboratory of Christopher C. Barney, PhD studying the role of the renin-angiotensin system within the brain in cardiometabolic adaptations of animals to hot environments. As an undergraduate, Dr. Grobe also worked for a short time in the laboratory of Neil E. Rowland, PhD at the University of Florida’s Department of Psychology (Gainesville, FL), studying the influence of angiotensin signaling in the forebrain in the thermoregulatory and behavioral effects of ethanol. He then completed his PhD training in Pharmacodynamics at the University of Florida’s College of Pharmacy, working in the laboratory of Michael J. Katovich, PhD and in collaboration with Mohan K. Raizada, PhD to understand the role of enzymes and peptides of the renin-angiotensin system that had only recently been discovered (such as angiotensin converting enzyme-2 (ACE2) and its product, angiotensin-(1-7)) in cardiac remodeling during chronic hypertension. Dr. Grobe then moved to the University of Iowa (Iowa City, IA) for postdoctoral training with Curt D. Sigmund, PhD, and began working to understand the role of angiotensin signaling within the hypothalamus in the control of blood pressure and metabolism. Dr. Grobe was hired onto the faculty at the University of Iowa, Department of Pharmacology, as an instructor in 2010. He started on the tenure track as an Assistant Professor in 2012, and was simultaneously tasked with helping to set up a metabolic phenotyping core facility within the Fraternal Order of Eagles’ Diabetes Research Center at the University of Iowa. He was promoted to Associate Professor with Tenure in 2017. In 2019, Dr. Grobe was recruited to the Medical College of Wisconsin (Milwaukee, WI) as an Associate Professor with Tenure in the Department of Physiology and the Department of Biomedical Engineering. In addition, he was tasked with founding the MCW Comprehensive Rodent Metabolic Phenotyping Core (CRMPC) facility. He was promoted to Professor in 2023, and was awarded the Butenhoff Family Professorship in Cardiovascular Research in 2024.

Dr. Grobe’s research focuses on four complementary areas:

First, the team works to understand the neurocircuitry within the hypothalamus that coordinates blood pressure and metabolic control. We have discovered that the angiotensin AT1R receptor, expressed on a unique subtype of Agouti-related peptide (AgRP) neuron within the arcuate nucleus of the hypothalamus, is critically required for normal integrative cardiometabolic control. Ongoing work includes dissecting the connectome of these neurons, the intracellular signaling cascades that mediate AT1R signaling in the cell, and the mechanisms through which these cascades change during prolonged obesity. Ultimately, we hope to understand the pathogenesis of obesity-associated hypertension and to identify novel therapeutic targets to treat both obesity and hypertension.

Second, the team works to understand mechanisms that mediate life-long programming of cardiometabolic disease predisposition in babies that are born prematurely. Due to renal immaturity, preterm birth is associated with altered sodium homeostasis and a high risk of sodium depletion. We have discovered that this sodium depletion contributes to life-long changes in autonomic, cardiovascular, and metabolic control, and this appears to be mediated (at least in part) through the same neurocircuits that we are studying in the context of adult obesity-hypertension. Ultimately, we aim to understand and optimize clinical care for infants born prematurely, to prevent later cardiometabolic disease.

Third, the team works to understand molecular mechanisms that contribute to the pregnancy-associated cardiovascular disorder, preeclampsia. We have discovered that arginine vasopressin secretion from the hypothalamus precedes and is strongly predictive of the clinical manifestation of preeclampsia, and that low-dose infusion of this hormone into animal models is sufficient to cause preeclampsia-like phenotypes. Ongoing work is aimed at understanding why arginine vasopressin secretion is elevated months before the onset of preeclampsia, and how increased activity of associated G protein coupled receptor signaling within the placenta contributes to the development of this disorder. These discoveries have led to various patents describing methods to predict and to intervene in preeclampsia. Ultimately, we aim to identify additional novel diagnostics and therapeutic targets for this devastating disorder.

Fourth, the team works to develop novel technologies for assessing metabolic rate (uniquely including anaerobic metabolism) in live rodents. This technology development bolsters ongoing work investigating the bioenergetic flux of the gut microbiota, which represents a large and woefully unappreciated contributor to total body energy flux. Ultimately, we aim to commercialize our novel equipment, and thereby improve cardiometabolic phenotyping approaches and accelerate discovery of novel therapeutic modalities for hypertension and obesity.