BIOGRAPHICAL SKETCH
NAME
POSITION TITLE
Heinrich Taegtmeyer, MD, DPhil
Professor of Medicine
eRA COMMONS USER NAME HTaegtmeyer
EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, and include postdoctoral training.)
INSTITUTION AND LOCATION
University of Freiburg i.Br., Germany
Harvard Medical School, Boston, MA
University of Oxford, England
DEGREE
(if applicable)
YEAR(s)
Dr. med.
1968
D.Phil.
1971-76
1981
FIELD OF STUDY
Medicine
Medicine/Cardiology
Metabolism
A. Personal Statement
The focus of my laboratory is cardiac metabolism in the broadest sense: Regulation of energy substrate
metabolism in the normal and diseased heart and metabolic signals which regulate pathways of intracellular
protein synthesis and degradation. In gain-of-function and loss-of-function models we recently acquired insight
into metabolic determinants by which heart muscle cells renew themselves from within by taking down
damaged (useless) proteins and by replacing those with new (functional) proteins. We have strong evidence
suggesting that metabolic signals regulate this process. The consequences of metabolic dysregulation on
protein turnover in the heart are of special interest. The aim is to integrate cardiac metabolism into the
molecular biology of the heart, and we have all the tools to do it. These tools include the precise
measurements of intra- and extra-cellular metabolic concentrations. I have a demonstrated record of
successful and productive metabolic research for over 30 years, and I have the support from a dedicated group
of young investigators, including graduate students and post-doctoral fellows. Lastly, I consider it a strength to
work with an experimental group of collaborators and consultants on the campus of the Texas Medical Center.
B. Positions and Employment
1968-70
1971-73
1971-76
1973-76
1976-79
1980-82
1982-87
1983-present
1987-91
1988-94
1989-present
1991-present
20112011-
Medizinalassistent, University of Freiburg i. Br., Germany
Jr./Sr. Assist. Resident, Harvard Medical Service, Boston City Hospital, Bosto n, MA
Clinical/Research Fellow in Medicine, Harvard Medical School, Boston, MA
Fellow, Cardiovasc. Div., Dept. Med., Peter Bent Brigham Hospital, Boston, MA
Instructor in Medicine at the PBBH, Harvard Medical School, Boston, MA
Hon. Research Registrar (Senior Registrar), Dept. Cardiovasc. Med., Oxford,
England
Assistant Professor of Medicine, The University of Texas Medical School at
Houston
Faculty, Graduate School of Biomedical Sciences, The University of Texas-Houston
Health Science Center
Associate Professor of Medicine, The University of Texas Medical School at
Houston
Director, Fellowship Program in Cardiovascular Medicine, The University of Texas
Medical School at Houston
Co-director, Division of Cardiology, The University of Texas Medical School at
Houston
Professor of Medicine, The University of Texas Medical School at Houston
Adjunct Professor, Department of Medicine, Baylor College of Medicine, Houston, TX
Co-Director, Metabolomics Core Laboratory, Baylor College of Medicine, Houston, TX
Awards and Other Professional Activities
Studienstiftung des Deutschen Volkes. Dr. med. summa cum laude, University of Freiburg, Germany
(1968); Byk Gulden Award, University of Freiburg, Germany (1968); American Board of Internal
Medicine (1974); Subspecialty Board in Cardiovascular Disease (1977); Lyndon B. Johnson Award,
American Heart Assn., Texas Affiliate (1983); Alpha Omega Alpha (1992); Fellow of the American
College of Cardiology, the American Heart Assn., and the International Society for Heart Research;
Research Allocation and Advisory Committee, AHA Texas Affiliate (1984-92); NIH Special Study
Sections (1985-2005); Dean’s Teaching Excellence List, University of Texas Houston Medical School
(1987-2000); Chair, Faculty Senate, University of Texas Houston Medical School (1988 -89); AHA
Cardiovasc. Physiol. Pathophysiol. Res. Study Committee (1989-91); President, Society for Heart and
Vascular Metabolism (2006-09); NIH Metabolism Study Section (1989-93); Review Committee, Nuclear
Medicine Program, US Dept. of Energy (1992); NIH Study Sections ad hoc yearly (1994-2013);
Distinguished Scientist Award, St. Luke’s Episcopal Hosp., Houston (2012); Associate Editor, Circulation
(1993-2004); Associate Editor, Cardiology (2002-Present); Editorial Board - Circ Res (1993-present), J.
Molec. Cell. Cardiol. (1993-present), Am. J. Physiol., Heart and Circ. Physiol. (1993-2010); J Am Coll
Cardiol (2010-present)
C. Selected Peer-reviewed Publication (from 250 peer-reviewed papers)
1. Razeghi P, Baskin KK, Sharma S, Young ME, Stepkowski S, Essop M, Taegtmeyer H. Atrophy,
hypertrophy and hypoxemia induce transcriptional regulators of the ubiquitin proteasome system in the rat
heart. Biochem Biophys Res Commun 2006; 342:361-364. PMID: 16483544
2. Sharma S, Adrogue J, Golfman L, Lemm J, Youker K, Noon GP, Frazier OH, Taegtmeyer H.
Intramyocardial lipid accumulation in the failing human heart resembles the lipotoxic rat heart.
FASEB J 2004; 18:1692-1700. PMID: 15522914
3. Dewald O, Sharma S, Adrogue J, Salazar R, Duerr GD, Crapo JD, Entman ML, Taegtmeyer H.
Dowregulation of PPARα-activated receptor-α gene expression in a mouse model of ischemic
cadiomyopathy is dependent on reactive oxygen species and prevents lipotoxicity. Circulation 2005;
112:407-15. PMID: 16009788
4. Razeghi P, Buksinska-Lisik M, Palanichamy N, Stepkowski S, Frazier OH, Taegtmeyer H.
Transcriptional regulators of ribosomal biogenesis are increased in the unloaded heart. FASEB J
2006; 20:1090-1096. PMID: 16770008
5. Razeghi P, Wang ME, Youker KA, Golfman L, Stepkowski S, Taegtmeyer H. Lack of NF-kappaB1
(p105/050) attenuates unloading-induced downregulation of PPAR-alpha and PPAR-alpha-regulated gene
expression in rodent heart. Cardiovasc Res 2007 74:133-139. PMID: 17276423
6. Sharma S, Guthrie P, Chan S, Haq S, Taegtmeyer H. Glucose phosphorylation is required for insulindependent mTOR signaling in the heart. Cardiovasc Res 2007; 76:71-80.
7. Wilson CR, Tran MK, Salazar KL, Young ME, Taegtmeyer H. Western diet, but not high fat diet, causes
derangements of fatty acid metabolism and contractile dysfunction in the heart of Wistar rats. Biochem J
2007; 406:457-67. PMID: 17550347
8. Leichman JG, Wilson EB, Scarborough T, Aguilar D, Miller CC, Yu S, Algahim MF, Reyes M, Moody FG,
Taegtmeyer H. Dramatic reversal of derangements in muscle metabolism and diastolic left ventricular
function after bariatric surgery. Am J Med. 2008; 121:966-73. PMID: 18954843
9. Kassiotis C, Ballal K, Wellnitz K, Vela D, Gong M, Salazar R, Frazier OH, Taegtmeyer H. Markers of
autophagy are downregulated in failing human heart after mechanical unloading. Circulation 2009; 120(11
Suppl):S191-7. PMID: 19752367
10. Harmancey R, Wilson CR, Wright NR, Taegtmeyer H. Western diet changes cardiac acyl-CoA
composition in obese rats: A potential role for hepatic lipogenesis. J Lipid Res 2010; 51:1380-93. PMID:
20093477
11. Li MV, Chen W, Harmancey R, Nuotio-Antar AM, Imamura M, Saha P, Taegtmeyer H, Chan L. Glucose6-phosphate mediates activation of the carbohydrate responsive binding protein (ChREBP). Biochem
Biophys Res Commun. 2010; 395:395-400 PMID: 20382127
12. Samudio I, Harmancey R, Fiegl M, Kantarjian H, Konopleva M, Korchin B, Kaluarachchi K, Bornmann W,
Duvvuri S, Taegtmeyer H*, Andreeff M*. Pharmacologic inhibition of fatty acid oxidation as a novel
therapeutic strategy for acute myeloid leukemia. J Clin Invest 2010; 120(1):142-56. *corresponding
authors. PMID: 20038799
13. Baskin KK, Taegtmeyer H. AMP-activated protein kinase regulates E3 ligases in rodent heart. Circ Res.
2011;109 1153-1161; PMID 21921267
14. Despa S, Margulies KB, Chen L, Knowlton AA, Havel PJ, Taegtmeyer H, Bers DM, Despa F.
Hyperamylinemia contributes to cardiac dysfunction in obesity and diabetes: A study in humans and rats.
Circ Res 2012; 110:598-608. PMC3303627
15. Harmancey R, Lam TN, Lubrano GM, Guthrie PH, Vela D, Taegtmeyer H. Insulin resistance improves
metabolic and contractile efficiency in stressed rat heart. FASEB J 2012 26:3118-3126; PMID 22611083
16. Reineke EL, York B, Stashi E, Chen X, Tsimelzon A, Xu J, Newgard CB, Taffet GE, Taegtmeyer H,
Entman ML, O'Malley BW. SRC-2 co-activator deficiency decreases functional reserve in response to
pressure overload of mouse heart. PLoS One 2012;7(12):e53395. doi: 10.137/journal.pone0053395.
[Epub 2012 Dec 31]. PMID: 23300926
17. Sen S, Kundu BK, Wu HC, Hashmi SS, Guthrie P, Locke LW, Roy RJ, Matherne GP, Berr, SS, Terwelp
M, Scot B, Carranza S, Frazier OH, Glover DK, Dillmann, WH, Gambello MJ, Entman ML, Taegtmeyer H.
Glucose regulation of load-induced mTOR signaling and ER stress in mammalian heart. JAHA 2013 (in
press)
D. Research Support
Ongoing Research Support
NHLBI 2R01-HL-61483-10
PI – Dr. Heinrich Taegtmeyer
“Self-renewal of the Cardiomyocyte”
2011-2016
The work seeks to identify metabolic signals as regulators of myocardial protein turnover and seeks to broaden
the role energy substrate metabolism from a provider of ATP to a regulator of self-renewal of the
cardiomyocyte
1 R03 EB011576-01
(PI: Jane Grande-Allen, Rice University) 2011-2013 0.6 mos.
National Heart, Lung and Blood Institute of the NIH
“Tissue Engineering Strategies: Effects on Valvular Interstitial Cell Metabolism”
The objective is to determine how cytokines, hypoxia and dynamic mechanical stretch influence the
metabolism and gene expression of vascular interstitial cells in valve metabolism and tissue engineered
valves.
2 T32 Training Program Grants: Center for Clinical and Translational Sciences
(Mentor to Meredith Rees and Henry C. Wu)
12/2012 – 11/2013
Title of Rees Project: “Metabolic Basis of Sunitinib Induced Cardiac Toxicity”
The proposed work will elucidate the mechanism of sunitinib-induced metabolic dysregulation and cardiac
dysfunction with the ultimate goal of identifying drugable targets for adjunct therapy in patients. We propose
that PDGFRβ inhibition leads to a flooding of the heart muscle cell with glucose substrate.
Title of Wu Project:
“Metabolic Dysregulations and Modulations of a Genetic Model of Herat Failure”
The proposed work will expose important interaction of PDFGRβ signaling pathways with metabolic regulators
in the heart. This will not only aid in the development of strategies to prevent cardiotoxicity due to tyrosine
kinase inhibitors but also provide novel insights to the role of PDGFRβ signaling in the failing heart.
Completed Research
NHLBI 5RO1 HL073162-05
“Glucotoxicity and Cardiac Dysfunction in Obesity”
PI – Dr. Heinrich Taegtmeyer
2003-2009
The objective of this grant was to determine whether metabolic dysregulation of glucose and fatty acid
metabolism in the heart is cause, rather than consequence, of contractile dysfunction in clinically severe
obesity.
T32 Training Program: Center for Clinical and Translational Sciences
University of Texas Health Science Center
4/1/2010–3/31/2012
Mentor to Shiraj Sen, MD/PhD Candidate
“Metabolic Signals as Regulators of Cardiac Growth Pathways”
This work seeks to identify energy substrate metabolism as a potential target of pharmacological agents for
improving function of the failing heart. If successful, we will have paved the way for a novel, more targeted
approach to preventing the progression of or treating the underlying metabolic derangements of heart failure.
American Heart Association
Mentor to Kedryn Baskin, PhD Candidate
1/1/2011-12/31/2011
Pre-doctoral Fellowship
“AMPK Regulates Ubiquitin Ligases in Cardiomyocytes”
This work sought to establish whether the activation of AMPK is necessary and sufficient to increase
Mafbx/Atrogin-1 and MuRF-1 expression in cardiomyocytes both in vitro and in vivo. We also seek to reveal
whether AMPK activation regulates MEF2-DNA binding and MEF2 transcription of MuRF-1 in the heart.
American Heart Association
Mentor to Dr. Romain Harmancey
Post-doctoral Fellowship
“Cardioprotective Effects of Insulin Resistance”
7/1/09-6/30/11
Our long-term goals were to demonstrate that insulin resistance is adaptive and beneficial for cardiac function,
and to define the conditions in which this beneficial effect becomes maladaptive. The findings will offer a new
perspective on insulin resistance as a protective mechanism for the heart. Ultimately, we will develop a
rationale for new strategies to prevent and treat heart failure in diabetes.
Mentor to Howard Hughes Medical Institute Research Fellow:
Kari Wellnitz
7/1/2008-6/30/2009
Mentor to Fellow
“Metabolic Stress of Type 2 Diabetes Induces Autophagy”
The goal was to determine the effect of diabetes on the levels of autophagy in the myocardium and determine
if failing hearts of Type 2 diabetic patients display increased levels of autophagy in response to mechanical
unloading.