Jefferson receives $11.6M NIH grant to study novel mechanisms of hea...( (PHILADELPHIA) Scientists at Jeffe...)

(PHILADELPHIA) Scientists at Jefferson Medical College have received a five-year, $11.6 million grant from the National Heart, Lung and Blood Institute to study molecular mechanisms of cardiac injury that lead to heart failure and potential repair processes that occur in the adult failing heart. This project aims to find data that can be translated into novel therapeutic strategies to improve the failing heart.

This study is unique in that were not only studying factors that contribute to heart failure but we are also looking for cellular and molecular mechanisms that promote repair for the damaged heart, said principal investigator Walter J. Koch, PhD., the W.W Smith Professor of Medicine and director of the Center for Translational Medicine in the Department of Medicine at Jefferson Medical College of Thomas Jefferson University. We will have four core facilities and four different labs working on this grant from a host of different angles. While much of the project will focus on the science of failure and repair, it is also clinically relevant in that we are working with stem cells and pharmaceutical drugs already being given to patients.

An advantage of this type of NIH Program Project Grant is that the four primary projects can be supported by core units. This grant supports four core areas: administrative, surgical, molecular and gene therapy and four main laboratories. In addition to Dr. Kochs leadership in these areas, leaders of these facilities are Andrea Eckhart, Ph.D., Patrick Most, M.D., Erhe Gao, M.D., Ph.D. and Joseph Rabinowitz, Ph.D., all faculty members in the Center for Translational Medicine.

Dr. Kochs group is studying how the enzyme GRK5, which plays a novel role in heart cell signaling and function, is involved in regulating heart cell gene transcription. Gene transcription is part of the two-step process that cells use to read a gene and produce a protein. According to Dr. Koch, abnormal increases in gen
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