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Hall Biosketch

BIOGRAPHICAL SKETCH

NAME: John E. Hall, Ph.D.
eRA COMMONS USER NAME (credential, e.g., agency login): johnehall
POSITION TITLE: Arthur C. Guyton Professor & Chair; Director, Mississippi Center for Obesity Research
EDUCATION/TRAINING

A. Personal Statement

My major research contributions have been in the general fields of cardiovascular and renal diseases, mechanisms of hypertension and target organ injury, obesity and metabolic disorders. Current research in our laboratory is focused on mechanisms of obesity and cardiorenal injury, heart failure, central nervous system mechanisms of obesity-induced hypertension, and how the molecular signaling pathways that regulate appetite, energy expenditure and sympathetic activity are altered in obesity. Our lab uses genetic, molecular, integrative physiological, and translational approaches in our research studies and we have extensive experience in cardiovascular, renal and metabolic phenotyping. My contributions to science include 24 books and >640 scientific publications. My research has been funded by NIH since 1975. I have served as PI of the NIH/NIGMS-funded Center for Biomedical Research Excellence (COBRE) grant (P20GM104357 and P30GM149404) for the past 11 years and as PI of a NHLBI-funded Program Project grant (P01HL51971) for 30 years. I also currently serve as Professional Development Core Director of a NIH/NIGMS funded Center for Clinical and Translational Research (U54GM115428) and co-investigator of 2 NIH R01 grants (R01DK121748, and R01HL163076). I have mentored over 150 postdoctoral fellows, graduate students, medical students and undergraduate students. At least 7 of my trainees have become chairs/directors of departments, two have become Dean/Vice Dean of Graduate School/Academic Affairs, and many are productive researchers at academic institutions.

B. Positions, Scientific Appointments, and Honors

Professional Experience (Selected)

Honors, Professional Society Leadership, Editorships (Selected)

C. Contributions to Science (selected from >640 publications)

Intrarenal actions of angiotensin II (Ang II) in regulating renal sodium reabsorption and blood pressure. Our studies were among the first to demonstrate the importance of the direct intrarenal actions of Ang II in regulating renal sodium reabsorption, feedback regulation of glomerular filtration rate, and long-term blood pressure. These studies also first demonstrated the powerful role of the renin-angiotensin system in controlling salt-sensitivity of blood pressure.

1. Hall JE, Guyton AC, Jackson TE, Coleman TG, Lohmeier TE, Trippodo NC. Control of glomerular filtration rate by renin-angiotensin system. Am J Physiol 1977; 233: F366-372. PMID: 920806
2. Hall JE, Guyton AC, Smith Jr MJ, Coleman TG. Chronic blockade of angiotensin II formation during sodium deprivation. Am J Physiol 1979; 237: F424-432. PMID: 391063
3. Hall JE, Guyton AC, Smith Jr MJ, Coleman TG. Blood pressure and renal function during chronic changes in sodium intake: role of angiotensin. Am J Physiol 1980; 239: F271-F280. PMID: 6254369
4. Hall JE. Control of sodium excretion by angiotensin: intrarenal mechanisms and blood pressure regulation. Am J Physiol 1986; 250: R960-R972. PMID: 3521337

Role of kidneys and pressure natriuresis in long-term control of blood pressure and in hypertension. Our laboratory was the first to experimentally demonstrate that the kidney’s ability to excrete salt and water, via renal-pressure natriuresis, plays a crucial role in long-term control of blood pressure and in maintaining salt and water balance in several forms of hypertension.

1. Hall JE, Granger JP, Hester RL, Coleman TG, Smith Jr MJ, Cross RB. Mechanisms of "escape" from sodium retention during angiotensin II hypertension. Am J Physiol 1984; 246: F627-F634. PMID: 6720967
2. Hall JE, Granger JP, Smith Jr MR, Premen AJ. Role of renal hemodynamics and arterial pressure in aldosterone "escape". Hypertension 1984; 6 (Suppl. I): I183-I192. PMID: 6724669
3. Hall JE, Granger JP, do Carmo JM, da Silva AA, Dubinion J, George E, Hamza S, Speed J, Hall ME. Hypertension: physiology and pathophysiology. Comprehensive Physiology 2012; 2: 2393-2442. PMID:23720252
4. Hall JE. Kidney dysfunction, rather than non-renal vascular dysfunction, mediates salt-induced hypertension. Circulation 2016; 133: 894-907. PMID: 26927007

Mechanisms of obesity-induced hypertension and target organ injury. Our research demonstrated a key role for abnormal kidney function caused by intrarenal and perirenal fat, activation of mineralocorticoid receptors, and activation of the sympathetic nervous system in causing obesity-induced hypertension. We also demonstrated that obesity is associated with glomerular hyperfiltration, mitochondrial and endoplasmic reticulum dysfunction, renal injury and cardiac dysfunction even before development of severe hypertension and diabetes.

1. Hall JE. The kidney, obesity, and hypertension. Hypertension 2003; 41: 625-633. PMID: 12623970
2. Hall JE, do Carmo JM, da Silva AA, Wang Z, Hall ME. Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms. Circulation Res 2015; 116: 991-1006. PMID: 25767285
3. Hall JE, do Carmo JM, da Silva AA, Wang Z, Hall ME. Obesity, kidney dysfunction and hypertension: Mechanistic links. Nature Reviews Nephrology 2019; 15: 367-385. PMID:31015582
4. Hall JE, Mouton A, da Silva AA, Omoto ACM, Wang Z, Li X, do Carmo JM. Obesity, kidney dysfunction and inflammation: interactions in hypertension. Cardiovasc Res. 2021; 117: 1859-1976. PMID: 33258945

Role of central nervous system leptin-proopiomelanocortin system in long-term blood pressure regulation, hypertension, obesity, and target organ injury. Our laboratory discovered that increases in leptin, a hormone secreted by fat cells, cause chronic increases in blood pressure, providing a partial explanation for why obesity causes hypertension. Moreover, we demonstrated that leptin-induced hypertension is due to stimulation of the sympathetic nervous system. We also used genetic engineering methods to determine how fat cells communicate with the brain to differentially regulate metabolic and cardiovascular functions. Our lab also discovered that chronic melanocortin 4 receptor (MC4R) activation causes hypertension via sympathetic activation and that leptin-induced hypertension and antidiabetic actions are mediated through stimulation of proopiomelanocortin neurons and subsequent activation of MC4R. We also discovered that activation of the central nervous system leptin-melanocortin pathway confers remarkable protection against progressive heart failure following severe myocardial infarction and that the beneficial cardiac protective actions of leptin require activation of brain melanocortin-4 receptors. These findings highlight a potentially novel therapeutic approach for myocardial infarction and heart failure.

1. Hall JE, daSilva AA, doCarmo JM, Dubinion J, Hamza S, Munusamy S, Smith G, Stec D. Obesity-induced hypertension: role of sympathetic nervous system, leptin and melanocortins. J Biol Chem 2010; 285: 17271-17276. PMID: 20348094
2. do Carmo JM, da Silva AA, Cai Z, Dubinion JH, Hall JE. Control of arterial pressure, appetite and glucose by leptin in mice lacking leptin receptors in POMC neurons. Hypertension 2011; 57: 918-926. PMID: 21422382
3. da Silva AA, Freeman JN, Hall JE, do Carmo JM. Control of appetite, blood glucose and blood pressure during chronic melanocortin-4 receptor activation in normoglycemic and diabetic NPY deficient mice Am J Physiol: Regulatory, Integrative and Comparative Physiology 2018; 314: R533-R539. PMID: 29351428
4. Omoto ACM, do Carmo JM, Nelson B, Aitkem N, Dai X, Flynn E, Wang Z, Li X, Hall JE, da Silva AA. Central nervous system actions of leptin improve cardiac function independent of sympathetic innervation after ischemia-reperfusion. J Am Heart Assoc. 2022 Nov;11(21):e027081. doi: 10.1161/JAHA.122.027081. Epub 2022 Oct 27. PMID: 36300667

Heart Failure – role of central nervous system mechanisms, inflammation, and new therapeutic approaches. Our laboratory discovered new pathways for cardiac protection mediated via the central nervous system after myocardial infarction as well as in as in obesity and hypertension. These studies highlight promising new therapeutic approaches for treatment of myocardial infarction and heart failure.

1. Mouton AJ, Li X, Hall ME, Hall JE. Obesity, hypertension and cardiac dysfunction: novel roles of immunometabolism in macrophage activation and inflammation. Circulation Research 2020; 126: 789-806. PMID: 32163341
2. Mouton AJ, Hall JE. Novel roles of immunometabolism and non-myocyte metabolism in cardiac remodeling and injury. Am J Physiol: Reg Integ Comp Physiol 2020; 319: R476-R484. PMID: 32877243
3. Gava FN, da Silva AA, Dai X, Harmancey R, Ashraf S, Omoto ACM, Salgado M, Moak SP, Hall HE, do Carmo JM. Restoration of cardiac function after myocardial infarction by chronic activation of the CNS leptin-melanocortin system. J Am Coll Cardiology: Basic Translational Science 2021; 6: 55-70. PMID: 33532666
4. Li X, Lu Q, do Carmo JM, Wang Z, da Silva AA, Mouton A, Omoto ACM, Hall ME, Li J, Hall JE. Direct cardiac actions of the sodium glucose co-transporter 2 inhibitor empagliflozin improve myocardial oxidative phosphorylation and attenuate pressure-overload heart failure. J Am Heart Assoc 2021 Mar 16;10(6):e018298. doi: 10.1161/JAHA.120.018298. PMID: 33719499

Published Work Listed in MyBibliography:

https://www.ncbi.nlm.nih.gov/myncbi/john.hall.1/bibliography/public/