G
Garret A. FitzGerald
Researcher at University of Pennsylvania
Publications - 573
Citations - 64984
Garret A. FitzGerald is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Prostacyclin & Thromboxane. The author has an hindex of 127, co-authored 547 publications receiving 60448 citations. Previous affiliations of Garret A. FitzGerald include French Institute of Health and Medical Research & Brigham and Women's Hospital.
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State of the art: Atherosclerosis in a limited edition
TL;DR: Two new mouse models closely mimic human atherosclerosis, providing exciting opportunities for elucidating the molecular mechanisms of this disease and for evaluating novel therapeutics.
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The roles of lipids in SARS-CoV-2 viral replication and the host immune response.
TL;DR: In this paper, the authors summarize the existing literature on the mechanisms through which these lipid mediators may regulate viral burden in COVID-19 and identify the core areas in which lipids offer therapeutic promise for SARS-CoV-2.
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Knitting up the raveled sleave of care.
Guangrui Yang,Georgios K. Paschos,Anne M. Curtis,Erik S. Musiek,Sarah McLoughlin,Garret A. FitzGerald +5 more
TL;DR: This Review is based on the Franklin Epstein Lecture delivered at Beth Israel Deaconess Hospital on 25 April 2013 and discusses recent advances in the understanding of molecular clocks and highlight their relevance to human physiology and disease.
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Biopharmaceutical characterisation of a low‐dose (75 mg) controlled‐release aspirin formulation
William N. Charman,Susan A. Charman,Donald C. Monkhouse,Steven Edgar Frisbee,Earle A. Lockhart,Steven Weisman,Garret A. FitzGerald +6 more
TL;DR: The release of aspirin from a 75 mg controlled-release formulation, designed to inhibit maximally thromboxane A2 production while sparing stimulated prostacyclin biosynthesis, was characterised in healthy subjects.
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Simply read: erythrocytes modulate platelet function. Should we rethink the way we give aspirin?
TL;DR: In vitro observations of RBC-platelet interactions into the clinical domain are extended and suggest that interactions among platelets, RBCs, and PMNs may also facilitate the transcellular metabolism of bioactive lipids to novel species.