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Ryan A. Frieler

Researcher at University of Michigan

Publications -  16
Citations -  1082

Ryan A. Frieler is an academic researcher from University of Michigan. The author has contributed to research in topics: Myeloid & Inflammation. The author has an hindex of 10, co-authored 15 publications receiving 874 citations.

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Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice

TL;DR: It is shown that myeloid MR is an important control point in macrophage polarization and that the function of MR on myeloids cells likely represents a conserved ancestral MR function that is integrated in a transcriptional network with PPARgamma and glucocorticoid receptor.
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Immune Cell and Other Noncardiomyocyte Regulation of Cardiac Hypertrophy and Remodeling

TL;DR: It is now clear that intercellular signaling and communication between these cell types are critical in the pathophysiology of ventricular hypertrophy and remodeling, and there is still much to be revealed about the specific roles of these celltypes and their overall contribution to the hypertrophic response.
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Coxibs interfere with the action of aspirin by binding tightly to one monomer of cyclooxygenase-1

TL;DR: It is predicted that the cardioprotective effect of low-dose aspirin on COX-1 may be blunted when taken with coxibs, and administration of celecoxib to dogs interferes with the ability of a low dose of aspirin to inhibit AA-induced ex vivo platelet aggregation.
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Myeloid-Specific Deletion of the Mineralocorticoid Receptor Reduces Infarct Volume and Alters Inflammation During Cerebral Ischemia

TL;DR: The data demonstrate that myeloid MR activation exacerbates stroke and identify myeloids MR as a critical target for MR antagonists, and indicate that MR activation has an important role in controlling immune cell function during the inflammatory response to stroke.
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Neutrophils Restrict Tumor-Associated Microbiota to Reduce Growth and Invasion of Colon Tumors in Mice

TL;DR: Bacteria in tumors are found to induce production of IL17, which promotes influx of intratumor B cells that promote tumor growth and progression in mice with inflammation-induced and sporadic colon tumors.