The St. Hilaire Lab is seeking a highly motivated Postdoctoral Fellow to investigate the molecular mechanisms driving Medial Arterial Calcification (MAC), a distinct cause of peripheral artery disease (PAD) independent of atherosclerosis. This research builds upon groundbreaking work identifying mutations in CD73 as the cause of a rare MAC disorder. The project explores how genotoxic stress and the loss of DNA repair enzymes, such as Ercc1, trigger a signaling cascade that represses CD73 expression, disrupts vascular homeostasis, and initiates the transition of smooth muscle cells (SMCs) toward a bone-like phenotype. The successful candidate will lead experimental efforts to elucidate the contribution of the DNA damage response (DDR) to MAC and expand the study to investigate how cardiovascular calcification is accelerated by the unique stressors of deep space, such as radiation and microgravity. This role is centered on defining how cellular responses to DNA damage promote pathological remodeling and evaluating these pathways as therapeutic targets.
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Job Type
Full-time
Career Level
Entry Level
Education Level
Ph.D. or professional degree