Cynthia St. Hilaire, PhD, FAHA is an Associate Professor of Medicine, Division of Cardiology, at the University of Pittsburgh and a Faculty Scholar within the Vascular Medicine Institute. She leads a research team focused on identifying and characterizing the mechanisms underlying the development of vascular and valvular calcification pathologies, with specific interest in how inflammation and mechanical stress drive the transformation of a healthy vascular cell into a calcifying cell. For these investigations, the St. Hilaire Lab obtains human tissues from patients with various cardiovascular diseases, utilizes murine models and primary human patient cells and tissues to create in vitro and ex vivo disease models, and performs biochemical, molecular biology, and next generation sequencing techniques.
Education
- BA - 2001, University of Vermont
- PhD - 2008, Boston University School of Medicine
Research Interests
Research in the St. Hilaire Lab focuses on characterizing the underlying pathobiology of vascular disease, concentrating on mechanisms that drive vascular and valvular calcification and remodeling. Ectopic calcification in the cardiovascular system was once considered a passive and degenerative progression, but it is now appreciated that active biological processes drive this pathology, though the precise mechanisms inducing and propagating pathological calcification are not completely understood. Our overarching goal is to dissect the mechanisms that drive the transformation of a healthy vascular cell into a calcifying cell, in order to identify targets for the development of pharmacological therapies.
One avenue of research stems from the discovery by Dr. St. Hilaire and her colleagues at the NIH of the rare disease Arterial Calcification due to Deficiency of CD73 (ACDC). Patients with ACDC have inactivating mutations in the gene encoding for CD73, which catalyzes the breakdown of extracellular AMP to adenosine. ACDC patients exhibit severe medial-layer lower extremity vascular calcification and vessel tortuosity, which suggests that CD73 and adenosine signaling help to protect the vasculature from these pathologies. Vascular calcification and vessel tortuosity are phenotypes seen in a variety of diseases thus we aim to leverage what we learn from the study of this rare disease to identify novel mechanisms driving these pathologies in more common disorders.
Calcification in the aortic valves develops in roughly 30% of the aging population. Calcific aortic valve disease (CAVD) encompasses a spectrum of pathologic states that range from aortic sclerosis, the thickening and stiffening of the valve leaflets, to aortic stenosis, where blood flow to the aorta is obstructed and can lead to heart failure. We have created a human biospecimen bank of 150 control and CAVD valve specimens from which we obtain samples for pathology, biochemical, and gene expression analysis, as well as create primary cell lines that we use to study the process of how a healthy valve cell converts into a calcifying valve cell.
Please got to the St. Hilaire Lab website to learn more www.sthilairelab.pitt.edu