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Endothelial progenitor cells that reside in renal vasculature may be stimulated to initiate differentiation programs during episodes of injury. It is hypothesized that endothelial progenitor cells resident in the kidney can transition to a post-injury phenotype that promotes endothelial repair.
Endothelial dysfunction is central to the pathophysiology of vascular ischemia, bacterial sepsis, toxin-induced thrombotic microangiopathy, and antibody-mediated kidney transplant rejection and often manifest with renal failure. With each of these diagnoses circulating components of the complement cascade bind to endothelial cells and induce disease progression through anaphylactic cellular messaging, monocyte homing, and direct cell membrane disruption. In response to injury during embryologic development avascular metanephric blastema initiate endothelial differentiation. Although circulating hematopoietic progenitor cells have shown therapeutic promise they incorporate into renal vasculature at very low density.
Age
18 - 85 years
Sex
ALL
Healthy Volunteers
No
Brigham and Women's Hospital
Boston, Massachusetts, United States
Start Date
January 21, 2022
Primary Completion Date
December 30, 2023
Completion Date
December 30, 2024
Last Updated
August 3, 2022
Cell isolation
DIAGNOSTIC_TEST
Lead Sponsor
Brigham and Women's Hospital
NCT07460960
NCT07324902
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