Circulating activated platelets exacerbate atherosclerosis in mice deficient in apolipoprotein E

By Yuqing Huo, A. Schober, S. Forlow, David F. Smith, Matthew C. Hyman, Steffen Jung, Dan R. Littman, Christian Weber, Klaus Ley. Nature Medicine, 2003

1,109 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/90796b0a05a6d248472ee1a4eb0e07a4228ca435

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. A. Mócsai
2. A. Tedgui
3. A. Luster
4. R. Polanowska-Grabowska
5. S. Nourshargh
6. Klaus Ley
7. R. Alon
8. Z. Mallat

Citations in the corpus

• Platelet-neutrophil-interactions: linking hemostasis and inflammation. (2007, background): “The interaction between endothelial cells, platelets, and monocytes leads to in increased monocyte recruitment and accelerates the development of atherosclerotic lesions.(123) Therapeutic inhibition of leukocyte-platelet aggregates can mitigate inflammatory processes and thereby the development of a”
• Circulating Platelets as Mediators of Immunity, Inflammation and Thrombosis (2018, background): “Platelets may further contribute to atherogenesis through the delivery of proinflammatory factors to leukocytes and endothelial cells.81 The platelet-derived factors implicated in this setting are surface P-selectin and the platelet-derived chemokines RANTES and PF4.”
• The role of selectins in inflammation and disease. (2003, background): “Activated platelets deposit proinflammatory chemokines on the surface of endothelial cells and monocytes and accelerate atherosclerosis [ 42 ]; blockade or elimination of platelet P-selectin function reduces atherosclerosis in mouse models.”
• Atherosclerosis: current pathogenesis and therapeutic options (2011, background): “1 ), which are deposited by platelets or platelet-derived microparticles during their transient P-selectin–mediated interactions on inflamed endothelium, where they promote atherogenic monocyte arres”
• Cytokines in atherosclerosis: pathogenic and regulatory pathways. (2006, background): “In addition, activated platelets injected into apoE / mice enhance the development of atherosclerotic lesions compared with mice injected with the supernatant of activated platelets (298).”
• Getting to the site of inflammation: the leukocyte adhesion cascade updated (2007, background): “For example, platelets are known to deposit CC-chemokine ligand 5 (CCL5; previously known as RANTES), as well as other chemokines, such as CXC-chemokine ligand 4 (CXCL4) and CXCL5, onto the inflamed endothelium and thereby trigger the arrest of rolling monocyte”
• Diverse novel functions of neutrophils in immunity, inflammation, and beyond (2013, background): “…in atherosclerotic plaque formation (Massberg et al., 2002; Huo et al., 2003) and platelet-derived CCL5 was shown to promote monocyte adhesion to the luminal surface of early atherosclerotic lesions in the inflamed arterial wall in mice (von Hundelshausen et al., 2001; Huo et al., 2003).”