Mitra Esfandiarei, PhD

Assistant Professor

Midwestern University
College of Health Sciences
Biomedical Sciences Program
Cactus Wren 306-F
19555 N. 59 Ave.
Glendale, AZ  38305

Office: (623) 572-3666



B.S Microbiology Tehran University (Iran) 1988
M.S. Medical Microbiology Razi Vaccine & Serum Res. Inst. (Iran) 1998
M.S. Pathology & Lab Medicine Univ. of British Columbia (Canada) 2001
Ph.D. Pathology & Lab Medicine Univ. of British Columbia (Canada) 2006


Project I: Marfan Syndrome Associated Aortic Aneurysm

Marfan syndrome is a genetic disease caused by mutations in fibrillin-1, a large extracellular matrix glycoprotein that provides a scaffold for the formation and maturation of elastic fibers within the blood vessel wall and other connective tissues. Because of the weakening of the aortic wall, mortality in Marfan patients is usually due to progressive thoracic aortic aneurysm, dissection, and rupture. My laboratory is interested in understanding cellular mechanisms underlying aortic dysfunction and progressive aneurysm using both in vitro and in vivo models of Marfan associated aneurysm. We are interested in exploring cellular mechanisms involved in disease progression including the cross talk between the extracellular matrix, smooth muscle cells, and endothelial layer.

Project II: Endoplasmic Reticulum Stress Response & Vascular Dysfunction

Endoplasmic reticulum (ER) stress is a process resulting from the accumulation of unfolded proteins in within the ER lumen. The affected cell will attempt to alleviate the disruptive symptoms of stress by initiating the unfolded protein response (UPR). The UPR initiates a variety of processes, including increasing the concentration of certain chaperone proteins inside the ER, decreasing transcription and translation of new proteins, and increasing the degradation of misfolded proteins.  The effectiveness of these events will determine the cell's ultimate fate (survival or death). My laboratory is interested in answering important questions that address the changes in ER luminal calcium concentration that occur during the ER stress response in vascular smooth muscle and endothelial cells.


Complete List of Published Manuscripts

Published Book Chapter