Department of Cell Biology

Richard N. Kitsis, M.D. -- Research Interest

Kitsis


Professor, Departments of Cell Biology & Medicine
Office: Forchheimer G46
Lab: Golding Bldg., G01
718.430.2609

richard.kitsis@einstein.yu.edu

Research Interest 
Recent Publications 

 

   Key Words: cell death/apoptosis/necrosis/heart disease/cancer/diabetes

Cell Death: Fundamental Mechanisms and Roles in Human Disease: The most basic decision that any cell makes is to grow (proliferate or hypertrophy), differentiate, or die. Our laboratory is interested in the connections among these processes. A major focus is the fundamental mechanisms that mediate cell death and the role that cell death plays in key human diseases such as heart disease, cancer, and diabetes. We employ a variety of approaches including molecular and cellular biology, biochemistry, mouse and human genetics, and physiology. Key discoveries from the lab include: 1) First delineation of the role of regulated cell death in myocardial infarction (“heart attack”) and heart failure. 2) Recognition that death-fold motifs regulate cell death via non-homotypic, as well as conventional homotypic, interactions. 3) Elucidation of molecular mechanisms by which ARC, an endogenous inhibitor of apoptosis, antagonizes both extrinsic (death receptor) and intrinsic (mitochondrial/ER) death pathways. 4) Identification of critical roles for ARC in heart disease, breast cancer, and diabetes. 5) Recognition that Bax/Bak, classical regulators of apoptosis, also mediate necrosis. We are keen to translate these and other basic discoveries into clinical practice through structural anlayses and high throughput chemical screening.

Current areas of investigation
1. Evolutionary and mechanistic connections between apoptotic and necrotic cell death
2. Mechanisms by which Bax/Bak promote necrosis in myocardial infarction
3. Role of necrosis (not apoptosis) in cancer
4. Mechanisms linking death receptor and mitochondrial necrosis pathways
5. Mechanisms that mediate ARC degradation and apoptosis during heart disease
6. Regulation of ER stress-induced pancreatic β-cell death in diabetes
7. Role of ER-mitochondrial tethering by mitofusin 2 in cell death
8. Small molecule therapeutics for heart attacks based around manipulating Bax and ARC  
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