Research Interests
The Elrod laboratory is focused on two complimentary lines of research--the first being the identification of genetic components of mitochondrial calcium exchange and their role in cellular physiology and heart disease and the second being the utilization of genome-wide functional screening to discover novel modulators of the necrotic cell death program.
Heart failure and myocardial infarction, as well as many other diseases, are characterized by significant metabolic dysfunction and cell death, both of which have been shown to initiate and drive disease. Mitochondrial calcium signaling is a nexus for these processes regulating both oxidative phosphorylation (ATP production) and cell death. While much is known about how calcium exchange is regulated at the plasma membrane, our understanding of the mitochondrial calcium pool remains elementary. The lab utilizes in vitro and in vivo techniques including real-time measurements of calcium exchange in isolated cells and genetically engineered mice in clinically relevant disease models to dissect the molecular role of novel genes.
Historically, necrotic cell death (characterized by cell swelling, membrane rupture, lysis and inflammation) has largely been thought to be a non-specific-unprogrammed process and thereby void of distinct signaling events and genetic players. Recently, it has become clear that necrosis, like apoptosis, may be highly regulated and involve specific gene programs. To discover novel modulators of necrosis, we have utilized genome-wide functional screening in cell-based assay systems (shRNA lentiviral library). Using a "system biology" approach, we have identified unique players and pathways in cell death and are investigating their mechanisms of action.
The ultimate goal of the Elrod lab is to discover new therapeutic avenues for the treatment of disease with a focus towards myocardial infarction and heart failure.
Clinical Interests
Epithelial ovarian cancer (EOC) accounts for about 90% of ovarian cancers and represents the leading cause of gynecological cancer-related deaths. Recent studies show that EOC is a heterogeneous disease. High grade serous ovarian cancer (HGSOC) is the most common subtype that represents 70% of all EOC. The standard of care for women with HGSOC is the combination of platinum and taxane. However, the survival rates of these patients remain low due to the development of chemotherapeutic resistance and tumor recurrence. Therefore, new therapeutic options, such as targeted therapy, are required to improve the survival for EOC patients. Multiple epigenetic factors have high rates of amplification or overexpression in HGSOC patients. Subsets of HGSOC that are driven by impaired activity of epigenetic machinery are often characterized by poor prognosis. Thus, there is a great need for developing personalized therapeutic interventions that will target HGSOCs based on individual epigenetic landscape.
My research interest is focused on understanding the role of epigenetics in promoting tumorigenesis and chemoresistance in ovarian cancer. I am specifically interested in developing novel therapeutic strategies based on epigenetics that can potentially improve current standard-of-care therapies for ovarian cancer.
Education, Training & Credentials
- Kirschstein Fellow, Cincinnati Children's Medical Hospital, Howard Hughes Medical Institute, 2012 - Laboratory of Dr. Jeffrey Molkentin
- PhD, Pathology, Albert Einstein College of Medicine, 2007
- BS, Biology (cum laude), Centenary College, 2002
Memberships
- Basic Science Council, American Heart Association
- International Society for Heart Research
- American Physiological Society