Company:  Confidential

Job Title: Postdoc in the Cardiovascular Research Institute, at UCSF (Fidler Lab)

Job Number: 72261

Location: San Francisco, US

Job Description

The Fidler lab at the University of California San Francisco  is recruiting postdoctoral scientists to lead research projects centered on identifying fundamental mechanisms of atherosclerosis and thrombosis. This collaborative work will be conducted in the Cardiovascular Research Institute in San Francisco, CA. Postdoctoral Scholars will be eligible for generous benefits including supplemented health insurance and University housing in San Francisco

            The Fidler lab is centered on understanding how immune cells affect cardiovascular disease. Building off studies of large patient cohorts the Fidler lab utilizes animal models (primarily mice) of disease to understand pathogenesis. Current studies in the lab center on understanding the association between clonal hematopoiesis and cardiovascular disease. Immune cell communication with fibroblast and smooth muscle cells in atheromas and utilization of in vivo CRISPR screens to identify novel drivers of atherogenesis.


Clonal hematopoiesis is a highly prevalent condition in the elderly and occurs when somatic mutations arise in hematopoietic stem cells which instill a survival advantage. These mutations primarily occur in TET2, DNMT3A, ASXL1, JAK2, and PPM1D. People with clonal hematopoiesis have increased risk of cardiovascular disease including atherosclerosis. Studies in the Fidler lab are focused on understanding the fundamental mechanisms underlying the association between ASXL1 and PPM1D clonal hematopoiesis and cardiovascular disease.


Fidler TP, et. al. The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis. Nature. 2021.

Yu Z, et. al. Genetic Modification of Inflammation and Clonal Hematopoiesis-Associated Cardiovascular Risk. Journal of Clinical Investigation. 2023.


Two recent clinical trials have indicated that anti-inflammatory drugs can reduced cardiovascular disease. However, the fundamental mechanisms underlying this risk reduction are not well understood. Work in the Fidler lab has recently identified that macrophage inflammasome activation can mediate fibroblast accumulation in atheromas altering plaque stability. Work in the Fidler lab is centered on understanding if fibroblast are beneficial for atherosclerosis, and how they accumulate in lesions. These studies will be conducted in conjunction to in vivo CRISPR screens to identify novel drivers of pathogenesis.

Fidler TP, et. al. Suppression of IL-1b promotes beneficial accumulation of fibroblast-like cells in atherosclerotic plaques in clonal hematopoiesis. Nature Cardiovascular Research. 2024. 


Interested candidates should email their CV, a statement of research interest and contact information for three references to [Please click the Apply button for the link or email].

Application Deadline: 2024-03-02


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