This is an application for competitive renewal of an Institutional Training Grant entitled Mechanisms of Cardiovascular Diseases. Initially funded in July 1989, its mission is to provide training at the post-doctoral level in the area of molecular cardiovascular biology. The past 20 years has witnessed a veritable explosion in the application of cell and molecular biology and molecular genetics to the study of the cardiovascular system. In recent years, there has been considerable merging of these newer disciplines with classic biochemical, biophysical, and physiological approaches to the study of the cardiovascular system. The integration of these modalities makes it possible to begin to understand the precise mechanisms involved in complex processes such as congenital heart disease, atherosclerosis, ischemic heart disease, cardiac hypertrophy and failure, and arrhythmias and sudden death. Over 16 years ago, the Albert Einstein College of Medicine established one of the first Molecular Cardiovascular Programs in the nation to facilitate fundamental and translational cardiovascular research. This program has been very successful, leading to its expansion to 22 trainers working in 4 major areas: 1) Myocyte Growth, Differentiation, and Death; 2) Cardiovascular Development; 3) Intercellular Communication and Ion Channels; and 4) Vascular Growth and Response to Injury. This Institutional Training Grant supports Ph.D.s, M.D.s, and M.D./Ph.D.s pursuing conventional post-doctoral training and physicians in the Cardiovascular Fellowship Training Program who intend to pursue full time investigative careers. As a result of this program, dialogues among basic scientists, clinical cardiologists, cardiothoracic surgeons, and population scientists have been enhanced, leading to productive collaborations and cutting edge research. The years to come will undoubtedly continue to be exciting and informative with respect to cardiovascular diseases. Thus, this Institutional Training Grant is crucial to ongoing efforts to bring the considerable scientific depth of our institution to bear on problems of cardiovascular relevance.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Institutional National Research Service Award (T32)
Project #
Application #
Study Section
Special Emphasis Panel (ZHL1-CSR-G (F1))
Program Officer
Varghese, Jamie
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Albert Einstein College of Medicine
Internal Medicine/Medicine
Schools of Medicine
United States
Zip Code
Frunza, Olga; Russo, Ilaria; Saxena, Amit et al. (2016) Myocardial Galectin-3 Expression Is Associated with Remodeling of the Pressure-Overloaded Heart and May Delay the Hypertrophic Response without Affecting Survival, Dysfunction, and Cardiac Fibrosis. Am J Pathol 186:1114-27
Johnson, Simon C; Dong, Xiao; Vijg, Jan et al. (2015) Genetic evidence for common pathways in human age-related diseases. Aging Cell 14:809-17
Ebong, Eno E; Lopez-Quintero, Sandra V; Rizzo, Victor et al. (2014) Shear-induced endothelial NOS activation and remodeling via heparan sulfate, glypican-1, and syndecan-1. Integr Biol (Camb) 6:338-47
Ooi, Yaw Shin; Stiles, Katie M; Liu, Catherine Y et al. (2013) Genome-wide RNAi screen identifies novel host proteins required for alphavirus entry. PLoS Pathog 9:e1003835
Spray, David C; Hanstein, Regina; Lopez-Quintero, Sandra V et al. (2013) Gap junctions and Bystander Effects: Good Samaritans and executioners. Wiley Interdiscip Rev Membr Transp Signal 2:1-15
Gonzalez-Quesada, Carlos; Cavalera, Michele; Biernacka, Anna et al. (2013) Thrombospondin-1 induction in the diabetic myocardium stabilizes the cardiac matrix in addition to promoting vascular rarefaction through angiopoietin-2 upregulation. Circ Res 113:1331-44
Yang, Ying; Rodriguez, Jessica E; Kitsis, Richard N (2013) A microRNA links prolactin to peripartum cardiomyopathy. J Clin Invest 123:1925-7
Dai, Minxian; Freeman, Brandi; Shikani, Henry J et al. (2012) Altered regulation of Akt signaling with murine cerebral malaria, effects on long-term neuro-cognitive function, restoration with lithium treatment. PLoS One 7:e44117
Chen, Lu; Fu, Ya; Ren, Min et al. (2011) A RasGRP, C. elegans RGEF-1b, couples external stimuli to behavior by activating LET-60 (Ras) in sensory neurons. Neuron 70:51-65
Zaiman, Ari L; Damico, Rachel; Thoms-Chesley, Alan et al. (2011) A critical role for the protein apoptosis repressor with caspase recruitment domain in hypoxia-induced pulmonary hypertension. Circulation 124:2533-42

Showing the most recent 10 out of 41 publications