As a clinician-scientist, my goal is to investigate mechanistic determinants of human cardiovascular diseases. One of the primary objectives is to understand the mechanisms through which inflammatory and metabolic imbalance can contribute to disease progression in heart failure and cardiomyopathy. Specifically, our laboratory has investigated myeloperoxidase, ceruloplasmin, and dysregulated arginine metabolites, and cardiotonic steroids as mediators of nitrative stress in human heart failure, correlating physiologic alterations with metabolites and proteins measured by mass spectroscopy techniques or immunoassays in blood samples or enzyme expression in explanted human hearts. My laboratory has also extended efforts to understand how the heart interacts with other organs such as the kidneys and the lungs in the setting of heart failure. We are particularly interested in exploring counter-regulatory mechanisms that are operative to protect end-organ damage, which may provide clinical opportunity to identify future targets for preventive therapy. Areas of interest include high-density lipoprotein-associated paraoxonases, angiotensin-converting enzyme 2, dimethylarginine dimethylaminohydrolase (DDAH), and anti-inflammatory cellular autoimmune responses. As Clinical Core Director for the GeneBank at Cleveland Clinic and part of the collaborative Myocardial Applied Genomics Network (MAGNet), genetic, proteomic, and metabolomic links to pathogenic pathways in human heart diseases and heart failure are being explored. Research efforts are also conducted at the Clinical Research Unit with human subjects, using specific laboratory techniques to explore the clinical application of existing and novel biomarkers and/or imaging to link with physiologic understanding of the spectrum of human heart failure and cardiomyopathy.
As a clinician-scientist, the goal of my research is to investigate mechanistic determinants of cardiovascular disease, particular in human heart failure and cardiomyopathy. One of the primary objectives is to understand the mechanisms to which inflammation and cellular processes that promote disease progression, and the protective mechanisms that are operational to counteract these processes. The natural extension is to detect those at risk, thereby ultimately preventing the development of heart failure and cardiomyopathy.
Tang WH, Tong W, Troughton RW, et al. Prognostic Value and Echocardiographic Determinants of Plasma Myeloperoxidase Levels in Chronic Heart Failure. J Am Coll Cardiol 2007; 49: 2364-70.
Tang WH, Tong W, Shrestha K, et al. Differential Effects of Arginine Methylation on Diastolic Dysfunction and Disease Progression in Patients with Chronic Systolic Heart Failure. Eur Heart J 2008; 29: 2506-13.
Tang WH, Wang Z, Cho L, et al. Diminished Global Arginine Bioavailability as Metabolomic Profile of Increased Cardiovascular Risk. J Am Coll Cardiol 2009; 53(22): 2061-7.
Tang WH, Wu Y, Mann S, et al. Diminished Anti-oxidant Activity of High-Density Lipoprotein-Associated Proteins in Systolic Heart Failure. Circ Heart Fail 2011; 4:59-64.
Tang WH, Wu Y, Hartiala J, et al. Clinical and Genetic Association of Serum Ceruloplasmin with Cardiovascular Risk. Arterioscler Thromb Vasc Biol 2012; 32:516-22.
Tang WH, Wang Z, Levison BS, et al. Intestinal Microbiota Metabolism of Phosphatidylcholine and Incident Cardiac Risks. N Engl J Med 2012; in press.