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Dr. Georges E. Haddad

Georges Edmond Haddad, Ph.D.

Tenured Professor

  • Physiology & Biophysics
  • College of Medicine

Education & Expertise



Physiology and Biophysics
University of Sherbrooke


American University of Beirut, Lebanon


Cardiovascular Physiology & Electrophysiology

 Broadly, the laboratory of Dr. Haddad is involved in understanding the regulation of ionic channels (calcium and potassium) by intracellular signaling, leading to cellular modulation and organ dysfunction. In particular, Dr. Haddad has been investigating the novel role of cGRP in regulating intracellular signaling pathways in the modulation of the inotropic effects of the cardiomyocytes (in vitro) and the heart (in vivo), through alterations in the activity of ion channels and calcium dynamics. The role of PI3K/Akt pathways has been shown to play a significant role in determining cardiac stiffness and contractility in health and disease. In parallel, Dr. Haddad’s laboratory has been also heralding the work on the beneficial effects of low alcohol as well as the detrimental effects of high alcohol in the development of cardiac dysfunction and heart failure. We have found that alcohol activates the MAPKs and PI3K/Akt pathways, in a dose-independent manner and differentially during chronic versus acute exposure. This interplay was proven to be crucial for enhancing cardiac inotropy with low alcohol as well as the progression of alcoholic cardiomyopathy into failure with high alcohol exposure. Dr. Haddad’s laboratory is on the forefront of studying the interactions between these kinases to modulate ionic channels activities and survival, using in vivo and in vitro techniques from the molecular to the whole-animal level. In the same line, Dr. Haddad’s Lab has undertaken an important endeavor in linking a genetic fingerprint to alcoholic cardiomyopathy in human. Furthermore, Dr. Haddad’s laboratory was amongst the first to investigate the importance of PI3K/Akt and MAPK activations for survival during cardiac hypertrophy and failure, through regulation of ion channels activities. These studies showed strong novel correlation between potassium and calcium channels activities and dynamics with signaling expressions on the cardiac function. Such effects were found to corroborate with whole-animal cardiac dysfunctions in vivo, assessed through catheterization for pressure-volume relationship acquisitions. Such a realm of experience in electrophysiology, imaging, cellular and in vivo (whole-animal) ascertains our capacity and capability to fully invest in a new and interesting research direction towards HIV-research; starting with an exciting and novel project focusing on the effects of the combined retroviral therapy on the heart function.


Earlier Research:

In my early career as an independent investigator with expertise in electrophysiology, intracellular messengers as well as in-vitro and in-vivo physiological experimentation and animal model, I had a great interest in determining the regulation of cardiac contractility by protein kinases during the development of eccentric hypertrophy mainly using the accepted AV shunt model, developed in my post-doc laboratory. This initial endeavor led to the distinction of the hypertrophic compensatory mechanism from the early onset of the concealed molecular and functional defects at the sarcomere level. Other models for concentric hypertrophy were performed to assess the specificity of the signaling pathways vis-à-vis the hypertrophic model, both very relevant to human cardiac hypertrophic conditions:

1. Georges E. Haddad, Bernell R. Coleman, Aiqiu Zhao and Krista N. Blackwell (2004). Modulation of atrial contraction by PKA and PKC during the compensated phase of eccentric cardiac hypertrophy. Bas.Res.Cardiol., 99 (5), 317-327. 4. Tuanzhu Ha, Fang Hua, Yuehua Li, Jinag Ma, Xiang Gao, Jim Kelley, Aiqiu Zhao, Georges E. Haddad, David L. Williams, I. William Browder, Race L. Kao, and Chuanfu Li (2006). Blockade of MyD88 attenuates cardiac hypertrophy and decreases cardiac myocyte apoptosis in pressure overload induced cardiac hypertrophy in vivo. Am. J. Physiol. (Heart Circ. Physiol.): 290(3):H985-94.


2. Georges E. Haddad, Bernell R. Coleman, Aiqiu Zhao and Krista N. Blackwell (2005). Regulation of myocardial contraction by PKA and PKC during the development and regression of eccentric cardiac hypertrophy. Am. J. Phsyiol. (Heart Circ. Physiol.) 288: H695-H704

3. Tuanzhu Ha, Yuehua Li, Fang Hua, Jinag Ma, Xiang Gao, Jim Kelly, Aiqiu Zhao, Georges E. Haddad, David


L. Williams, I. William Browder, Race L. Kao, and Chuanfu Li (2005). Reduced cardiac hypertrophy in toll-like receptor 4-deficient mice following pressure overload. Cardiovasc. Res., 68: 224-234.

Genetic predisposition and the role of epigenetic factors in the development of cardiac pathologies became important parameters in the renewed interest of the cardiovascular scientific community in more individualized medicine and gene therapy. Thus, with the collaboration of leading cardiovascular scientist in the nation, I was able to lead significant studies in human hearts that highlighted the genetic profiling with specific cardiac diseases as published in the following papers:

1. Georges E. Haddad (2006). Gene therapy for treating diabetic cardiomyopathy: A new approach for a difficult clinical problem. Molecular Therapy, 13 (5): 835-838.

2. Georges E. Haddad, Lori Sanders, Seth Crosby, Maria Carles, et. al., and Judith K. Gwathmey (2008). Human cardiac specific cDNA array for idiopathic dilated cardiomyopathy: sex related differences. Physiological Genomics, 33 (2): 267-277.



3. Georges E. Haddad, Lori Sanders, Maria Carles, Seth Crosby, et. al., and Judith K. Gwathmey (2008). Fingerprint profile of alcohol-associated heart failure in human hearts. Alcoholism: Clinical and Experimental Research, 32 (5): 814-821. (Journal Media Highlight article).


In parallel, my research proceeded to further characterize the electrophysiological modulations during the development of cardiac hypertrophy based on our findings regarding the alterations in the kinase activities as well as pilot data showing the significant role of apoptotic pathways. Thus, we focused on the proliferation MAPK and the anti-apoptotic PI3K/Akt survival pathways. This led to novel findings regarding the modulation of ICa,L, IK, IK1 and IKATP by MAPK and PI3K. Most importantly, we were the first to document that these cardiac channels are differentially regulated by acute versus chronic MAPK and PI3K stimulation as depicted during the development of cardiac hypertrophy and its transition into failure:

1. Leyla Teos, Aiqiu Zhao, Zikiar Alvin, Graham G. Laurence, Chianfu Li, and Georges E. Haddad (2008). Basal and IGF-1-dependent regulation of potassium channels by MAP kinases and PI-3 kinase during eccentric cardiac hypertrophy. Am. J. Physiol. (Hrt Circ Physiol.) 295:H1834-H1845.

2. Aiqiu Zhao, Zikiar Alvin, Graham G. Laurence, Chuanfu Li, and Georges E. Haddad (2010). Cross-talk between MAPKs and PI-3K pathways alters the functional density of IK channels in hypertrophied hearts. Ethnicity & Disease. 20 (S1): 219-224.

3. Zikiar Alvin, Graham G. Laurence, Bernell R. Coleman, Aiqiu Zhao, Majd Hajj-Moussa, Georges E. Haddad (2011). Regulation of L-Type Inward Calcium Channels Activity by Captopril and Angiotensin II via the Phosphatidyl Inositol 3-Kinase pathway in Cardiomyocytes from volume-overload hypertrophied rat hearts. Can. J. Physiol. Pharmacol. 89 (3): 206 -215.

4. Zikiar Alvin, Graham G. Laurence, Bernell Coleman, Aiqiu Zhao, Majd Hajj-Moussa, Georges E. Haddad (2011). Regulation of the instantaneous inward rectifier and the delayed outward rectifier potassium channels by captopril and angiotensin II via the phosphoinositide-3 kinase pathway in volume-overload-induced hypertrophied cardiac myocytes. Medical Science Monitor 2011, BR 165-72.

5. ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume- Overloaded Rats (2011). Zikiar V. Alvin, Richard M .Millis, Wissam Hajj-Moussa, and Georges E. Haddad. Int. J. Cell. Biol., Vol. 2011, 838951.

6. Effects of IGF-1 on IK and IK1 Channels via PI3K/Akt Signaling in Neonatal Cardiac Myocytes. Richard Millis, Alvin Zikiar, Aiqiu Zhao and Georges E. Haddad (2012). Int. J. Cell. Biol., Vol. 2012, 712153.


A collaborative work on cGRP, a peptide known for its nociceptor activity and potent vascular, revealed for the first time that is has direct cardiac tonic in-vivo (PV-loop) and in-vitro effects that are partly mediated by PI3K. This can have a significant effect on future therapeutic use of cGRP agonist/antagonists. We will further our collaborative work on the gender difference of the cardiovascular cGRP effect and its alteration with aging (post-menopausal).

1. Gangula PR, Dong YL, Al-Hendy A, Richard-Davis G, Montgomery-Rice V, Haddad G, Millis R, Nicholas SB, Moseberry D (2013). Protective cardiovascular and renal actions of vitamin D and estrogen. Frontiers in Biosciences (Schol Ed.) 5:134-148.

2. Mustafa Al-Rubaiee, Pandu R. Gangula, Richard M. Millis, Georges E. Haddad (2013). Inotropic and Lusitropic effects of Calcitonin Gene-Related Peptide in the heart. AJP-Heart and Circ. Physiol. 304: H1525- H1537.

3. Nsini A. Umoh., Robin K., Richard M. Millis, Mustafa Al-Rubaiee M., Pandu Gangula, and Georges E. Haddad (2014). Calcitonin gene-regulated peptide regulates cardiomyocyte survival through regulation of oxidative stress by PI3K/Akt and MAPK signaling pathways. Annals of Clinical and Experimental Hypertension 2 (1): 1007-1032


A human pilot study in collaboration with exercise physiology team, revealed the importance of dietary nitrate in endurance and the cardiorespiratory functional capacity:

1. Vernon Bond Jr., Bryan H. Curry, Richard G. Adams, Richard M. Millis and Georges E. Haddad (2014). Cardiorespiratory function associated with dietary nitrate supplementation. Applied Physiology, Nutrition, and Metabolism 39(2): 168-172.

2. Richard M. Millis, Vernon Bond, Georges Haddad, and Richard Adams (2013). Oxygen consumption at 30 W of exercise is surrogate for peak oxygen consumption. ISRN Physiology, Volume 2013, Article ID 756276, 5.


The earlier genetic profiling work in alcoholic cardiomyopathy revealed genes of interest that could play a pivotal role in the clinically-proven transition of the beneficial low alcohol intake on the cardiac function into the detrimental cardiomyopathy with high doses. Thus, we have undertaken a major project from the molecular (gene and signaling molecules-oxidative stress and apoptotic), cellular (sarcomeric and cellular contraction, Intracellular Ca dynamics and ICa,L activities), tissue (immunohistochemistry and sterology) to the whole animal (PV-loop and echo), to elucidate the mechanisms involved in the transduction of the beneficial as well as the detrimental cardiac effects of alcohol in an acute (binge drinking) as well as chronic setting. Very interesting results showed that the dose dependent divergent effects of alcohol are due to divergent activation of different signaling pathways. Similar conclusions were drawn from the acute versus chronic alcohol study was performed. The use of adenoviral transfection in vivo as well as in vitro strengthen these findings. Future studies are aimed at assessing the alcoholic cardiac modulatory effects in conjunction with independent pathologies:

1. Robin K. Walker, Valeire M. Cousins, Nsini A. Umoh, Miara A. Jeffress, Delaram Taghipour, Mustafa Al - Rubaiee, Georges E. Haddad (2013). The good, the bad and the ugly with alcohol use and abuse on the heart. Alcoholism: Clinical and Experimental Research Journal 37 (8)1253-1260.

2. Nsini A. Umoh, Robin K. Walker, Mustafa Al-Rubaiee, Miara A. Jeffress, and Georges E. Haddad (2014). Acute alcohol modulates cardiac function as PI3K/Akt regulates oxidative stress. Alcoholism: Clinical and Experimental Research Journal 38 (7):1847-1864.

3. Morris NL, Ippolito JA, Curtis BJ, Chen MM, Friedman SL, Hines IN, Haddad GE, Chang SL, Brown LA, Waldschmidt TJ, Mandrekar P, Kovacs EJ, Choudhry MA. (2014). Alcohol and inflammatory responses: Summary of the 2013 Alcohol and Immunology Research Interest Group (AIRIG) meeting. Alcohol. 2014 S0741- 8329(14) 20160-1.



Structure Function - Cardiovascular Physiology

The Cardiovascular System Unit of the Structure and Function Unit 3 course of the 1st year Medical curriculum, Howard University (1999-2016).

Organ System Cardiovascular and Pulmonary Physiology

Pathophysiology of the Heart

Cardiac section of the Dental Physiology Course

Physiology & Pathophysiology of the cardiac system

Advanced Mammalian Physiology

Cardiovascular Physiology and Electrophysiology







  • NIH/NIGMS Grant T34GM149816; 4/1/2023-3/31/2028                        $1,469,595. 

Georges E. Haddad: External Collaborator (PI: Alvin Holder and Co-PI: Desh Ranjan).

Undergraduate Research Training Initiative for Student Enhancelment (U-Rise)


  • DC-CFAR; 1/1/2022-12/31/2024                                                              $50,000

     The effects of cART on the Heart.

     Georges E. Haddad: Principal Investigator


  • NIH/NIHMD Grant U54MD007597; 6/1/2019-1/31//2024                      $17,301,651

Georges E. Haddad: Director, Investigator Development Core (PI: William Southerland)

Percent effort: 1.2 Calendar months

Biomedical Infrastructure for Health Disparities Research (RCMI)


  • BFPSAP HUCOM 100214; 11/2016-11/2107                                          $20,985

Georges E. Haddad: Principal Investigator

Fetal alcohol exposure induced long-term cardiovascular impairment in middle-aged non-human primates


  • NIH/NIHMD Grant 8 G12MD007597; 7/2014-6/2019                            $10,055894

Georges E. Haddad: Director, Pilot Project Program      (PI: William Southerland)

Biomedical Infrastructure for Health Disparities Research (RCMI)


  • NIH/NIAAA grant 1R15AA019816-01A1; 9/2011-8/2015                      $442,002        

     Georges E. Haddad: Principal Investigator

     Mechanisms of Alcohol-induced Cardiomyopathy


  • NIH/NIGMS grant S06 GM008016-36;  9/2006-8/2012                          $1,100,000

     Program Director:  George K. Littleton

     Georges E. Haddad: Project Investigator.                                  

     Role of IGF-1 signaling and MAP Kinase in Cardiac Hypertrophy                                


  • NIH/NRCC/RCMI/RTRN grant SGP09-024; 12/2010-06/2012             $50,000

      Principle Investigator: Suzanne Porszasz-Reisz, Charles Drew University

      Georges E. Haddad: Collaborator.

Histological and Genetic Analysis of Muscle in COPD Patients


  • Mordecai-Whyatt Johnson grant 217512/U200043; 8/2007-7/2009         $100,000

     Georges E. Haddad: Principal Investigator.                              

     Role of MAPK in the progression of cardiac hypertrophy into heart failure.


  • NIHLB T32 Grant (HL073428-01), 8/2006-7/2009                                  $610,493

     Georges E. Haddad: Principle Investigator.                               

     Neural control of breathing and cardiovascular function.


  • NIH/NINDS grant NS039407-06A1; 9/2005-8/2011                                           

     Program Director: M. Haxhiu/J. Massari/Werner Graf

     Georges E. Haddad: Consultant.                                                

Central autonomic control: aging and oxidative stress


  • NIH/SCORE Grant (GM08016 33S1), 2003-2006                                   $686,639        

     Program Director:  George K. Littleton

     Georges E. Haddad: Project Investigator.                                  

     Cross talk between RAS and IGF-1 during eccentric cardiac hypertrophy. 


  • NIH/NRCC/RCMI grant 2G12 RR003048; 8/2006-7/2007                    $16,703          

Program Director: William Southerland

Georges E. Haddad: Project Investigator.                                 

Role of Nuclear Factor Kappa-B in the progression of cardiac hypertrophy into heart failure


  • NIH/NINDS grant 5U54NS39407-020004; 9/1999-8/2994

Program Director: Musa Haxhiu

     Georges E. Haddad: Consultant                                                                          

Gene regulatory mechanisms and neurogenic airway inflammation


  • Toby & Mort Mower Philanthropic Fund, 2000-2005.                             $137,000        

Georges E. Haddad: Principal Investigator.                             

Effect of Waveform Modification on Calcium Channels and intracellular Calcium Handling in Atrial Myocytes.                 


  • Howard University Funds for Academic Excellence Award, 2001-2002             $3,000

      Georges E. Haddad: Principal Investigator.                             

FASEB Summer Research Conference on Neuronal Mechanisms in Cardiovascular Regulation


  • Howard University Funds for Academic Excellence Award, 2000-2001             $3,000

     Georges E. Haddad: Principal Investigator.                              

     Medical Science Education Program


  • Howard University New Faculty Award, 1999-2001                                            $40,000          

     Georges E. Haddad: Principal Investigator.                              

Modulation of Ionic Currents during Development and Regression of Cardiac Hypertrophy: Role of ANG II and IGF-1”.



Post-Doctoral Fellow

Clinical Research Institute of Montreal, Experimental Hypertension and Vasoactive Peptides laboratory