Chemokine-driven transmigration of monocytes into the subendothelial space is a fundamental and rate- limiting process in atherogenesis. Our preliminary data show that this process is dysregulated by metabolic stress and that increased monocyte responsiveness to chemokines appears to accelerate atherosclerotic plaque development. We have now uncovered a novel thiol redox-sensitive mechanism in monocytes that upon dysregulation by metabolic disorders, 'primes' and transforms monocytes into a hyper-chemotactic pro- atherogenic phenotype.
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The University of Texas at San Antonio
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Southwest Research Institute
The University of Texas at San Antonio
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