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Faculty Detail    
Name TARIQ HAMID
Associate Professor
 
Campus Address SHEL 730 Zip 2182
Phone
E-mail  thamid@uabmc.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Medicine  Med - Cardiovascular Disease Associate Professor
Center  Comprehensive Cardiovascular Ctr  Comprehensive Cardiovascular Ctr Associate Professor

Biographical Sketch 
I am an Associate Professor of Medicine at the University of Alabama at Birmingham, Alabama. As a molecular biologist by training, I am interested in understanding the underlying molecular mechanisms related to cardiovascular pathologies such as ventricular remodeling and heart failure. The primary focus of my research is aimed at evaluating the role of inflammation and inflammatory signaling in the progression of such pathophysiology. I previously established the role of tumor necrosis receptors (TNFR) 1 and -2 in mediating ventricular remodeling responses and cardiac function in murine heart failure; specifically ablation of TNFR1 attenuates whereas ablation of TNFR2 promotes pathological ventricular remodeling. These effects were seen in part related to activation of transcription factor NF-kB. I later also reported that chronic activation of NF-kB induces detrimental LV-remodeling in a NF-kB-p65-subunit dependent manner. I have extensive expertise in analysis of molecular mechanisms underlying signal transduction pathways pertinent to cardiac remodeling and specially relating to cytokine-induced pathways. These studies over the course of years have paved the way for my current research. More recently, I have been actively pursuing studies aimed at analyzing inflammatory cell profiles in failing hearts and evaluating their roles in the progression of myocardial pathology. The long-term goal of these studies is to evaluate whether immune-cell modulation could be harnessed as a therapeutic avenue in alleviating HF in clinical settings. At the other end of the spectrum the lab also studies the role of cardiac mesenchymal stem cells (cMSCs) in myocardial fibrosis and regeneration, and establishing the mechanistic relationships between pathological inflammation and cMSC functional outcomes. Factors regulating normal stem-cell function and differentiation in the failing hearts are not clearly understood. Studies related to cMSCs are focused on evaluating the role of two important facets akin to failing hearts on the outcomes of cMSC function; 1) increased myocardial infiltration of monocyte/macrophages, and, 2) exaggerated myocardial fibrosis.

Society Memberships
Organization Name Position Held Org Link
Grant Reviewer: AHA National and Regional.     
Member of American Association for Cancer Research (2002-2005)     
Member of American Heart Association.      
Member of International Society for Heart Research     



Research/Clinical Interest
Title
Description
I am interested in studying the impact and influence of inflammatory mediators (immune cells, signaling pathways, cytokines and chemokines) on the functioning and therapeutic outcomes of cardiac stem cells in failing hearts. The research projects in the lab are focused on evaluating the molecular basis of cardiac stem cell functional outcomes and their interactions with the components of both innate and adaptive immune system.

Selected Publications 
Publication PUBMEDID
Immunomodulation Is the Key to Cardiac Repair  28495983 
CCR2+ Monocyte-Derived Infiltrating Macrophages Are Required for Adverse Cardiac Remodeling During Pressure Overload  30062209 
Dysfunctional and Proinflammatory Regulatory T-Lymphocytes Are Essential for Adverse Cardiac Remodeling in Ischemic Cardiomyopathy. Bansal SS, Ismahil MA, Goel M, Zhou G, Rokosh G, Hamid T, Prabhu SD  30586716  
Leukocyte iNOS is required for inflammation and pathological remodeling in ischemic heart failure. (2017)
Kingery JR, Hamid T, Lewis RK, Ismahil MA, Bansal SS, Rokosh G, Townes TM, Ildstad ST, Jones SP, Prabhu SD. 
28238121 
Mononuclear Phagocytes Are Dispensable for Cardiac Remodeling in Established Pressure-Overload Heart Failure. (2017)
Patel B, Ismahil MA, Hamid T, Bansal SS, Prabhu SD. 
28125666 
TNF receptor signaling inhibits cardiomyogenic differentiation of cardiac stem cells and promotes a neuroadrenergic-like fate. (2016) Hamid T, Xu Y, Ismahil MA, Jones SP, Bhatnagar A, Bolli R, Prabhu SD  27591224 
Remodeling of the Mononuclear Phagocyte Network Underlies Chronic Inflammation and Disease Progression in Heart Failure: Critical Importance of the Cardiosplenic Axis. (2013). Ismahil MA, Hamid T, Bansal SS, Patel B, Kingery JR, Prabhu SD.  24186967 
H2S protects against pressure overload-induced heart failure via upregulation of endothelial nitric oxide synthase. (2013). Kondo K, Bhushan S, King AL, Prabhu SD, Hamid T, Koenig S, Murohara T, Predmore BL, Gojon G Sr, Gojon G Jr, Wang R, Karusula N, Nicholson CK, Calvert JW, Lefer DJ.  23393010 
O-GlcNAc signaling is essential for NFAT-mediated transcriptional reprogramming during cardiomyocyte hypertrophy. (2012). Facundo HT, Brainard RE, Watson LJ, Ngoh GA, Hamid T, Prabhu SD, Jones SP.  22408028 
Chronic oral exposure to the aldehyde pollutant acrolein induces dilated cardiomyopathy. (2011). Ismahil MA, Hamid T, Haberzettl P, Gu Y, Chandrasekar B, Srivastava S, Bhatnagar A, Prabhu SD.  21908791 
Tumor necrosis factor receptor 2 signaling limits B-adrenergic receptor-mediated cardiac hypertrophy in vivo. (2011). Garlie JB, Hamid T, Gu Y, Ismahil MA, Chandrasekar B, Prabhu SD.  21691899 
Bovine model of doxorubicin-induced cardiomyopathy. (2011). Bartoli CR, Brittian KR, Giridharan GA, Koenig SC, Hamid T, Prabhu SD.  21253525 
Cardiomyocyte NFkB p65 promotes adverse remodelling, apoptosis, and endoplasmic reticulum stress in heart failure. (2011). Hamid T, Guo SZ, Kingery JR, Xiang X, Dawn B, Prabhu SD.  20797985 

Keywords
Inflammation, cardiac stem cells. myocardial Fibrosis