Why the study?
Blood clot formation initiates ischemic events, but the roles of coagulation during postischemic tissue repair are poorly understood.
Population
Mice subjected to hindlimb ischemia, primary endothelial cells, and patients with ischemic peripheral artery disease
Comparison
EPCR, PAR1, PAR2, or PAR4 deficiency, mutation, or agonism vs controls
Design
Preclinical in vivo and in vitro mechanistic study with human vascular and plasma samples
Authors
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May guide ischemia therapy development; leaves open translation from murine models to human disease.
Endothelial EPCR-PAR1 signaling supports postischemic neovascularization by suppressing hemoglobin expression and preserving nitric oxide bioavailability, identifying a novel link between coagulation signaling and tissue repair.
Bochenek et al. (2022) studied this question.
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