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• W2319345553 startingPage "125" @default.
• W2319345553 abstract "Vascular inflammation is a common cause of renal impairment and a major cause of morbidity and mortality of patients with kidney disease. Current studies consistently show an increase of extracellular vesicles (EVs) in acute vasculitis and in patients with atherosclerosis. Recent research has elucidated mechanisms that mediate vascular wall leukocyte accumulation and differentiation. This review addresses the role of EVs in this process. Part one of this review addresses functional roles of EVs in renal vasculitis. Most published data address anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis and indicate that the number of EVs, mostly of platelet origin, is increased in active disease. EVs generated from neutrophils by activation by ANCA can contribute to vessel damage. While EVs are also elevated in other types of autoimmune vasculitis with renal involvement such as systemic lupus erythematodes, functional consequences beyond intravascular thrombosis remain to be established. In typical hemolytic uremic syndrome secondary to infection with shiga toxin producing Escherichia coli, EV numbers are elevated and contribute to toxin distribution into the vascular wall. Part two addresses mechanisms how EVs modulate vascular inflammation in atherosclerosis, a process that is aggravated in uremia. Elevated numbers of circulating endothelial EVs were associated with atherosclerotic complications in a number of studies in patients with and without kidney disease. Uremic endothelial EVs are defective in induction of vascular relaxation. Neutrophil adhesion and transmigration and intravascular thrombus formation are critically modulated by EVs, a process that is amenable to therapeutic interventions. EVs can enhance monocyte adhesion to the endothelium and modulate macrophage differentiation and cytokine production with major influence on the local inflammatory milieu in the plaque. They significantly influence lipid phagocytosis and antigen presentation by mononuclear phagocytes. Finally, platelet, erythrocyte and monocyte EVs cooperate in shaping adaptive T cell immunity. Future research is needed to define changes in uremic EVs and their differential effects on inflammatory leukocytes in the vessel wall." @default.
• W2319345553 created "2016-06-24" @default.
• W2319345553 creator A5008276681 @default.
• W2319345553 creator A5022201775 @default.
• W2319345553 date "2016-01-01" @default.
• W2319345553 modified "2023-10-17" @default.
• W2319345553 title "Extracellular vesicles as mediators of vascular inflammation in kidney disease" @default.
• W2319345553 cites W114200782 @default.
• W2319345553 cites W1228803923 @default.
• W2319345553 cites W1519288303 @default.
• W2319345553 cites W1571704165 @default.
• W2319345553 cites W1637651838 @default.
• W2319345553 cites W1752938210 @default.
• W2319345553 cites W1838223162 @default.
• W2319345553 cites W184566394 @default.
• W2319345553 cites W1860926307 @default.
• W2319345553 cites W1890288585 @default.
• W2319345553 cites W1917940007 @default.
• W2319345553 cites W1925096404 @default.
• W2319345553 cites W1926299038 @default.
• W2319345553 cites W1935158033 @default.
• W2319345553 cites W1939008286 @default.
• W2319345553 cites W1952144636 @default.
• W2319345553 cites W1965056341 @default.
• W2319345553 cites W1965412752 @default.
• W2319345553 cites W1967979864 @default.
• W2319345553 cites W1968427762 @default.
• W2319345553 cites W1969627037 @default.
• W2319345553 cites W1969863654 @default.
• W2319345553 cites W1971219120 @default.
• W2319345553 cites W1971604855 @default.
• W2319345553 cites W1971725025 @default.
• W2319345553 cites W1972070926 @default.
• W2319345553 cites W1974041214 @default.
• W2319345553 cites W1974209230 @default.
• W2319345553 cites W1976622358 @default.
• W2319345553 cites W1976884472 @default.
• W2319345553 cites W1978209251 @default.
• W2319345553 cites W1980973980 @default.
• W2319345553 cites W1981975739 @default.
• W2319345553 cites W1983407800 @default.
• W2319345553 cites W1985138977 @default.
• W2319345553 cites W1986321004 @default.
• W2319345553 cites W1990635289 @default.
• W2319345553 cites W1990687389 @default.
• W2319345553 cites W1994240225 @default.
• W2319345553 cites W1995622771 @default.
• W2319345553 cites W1995890947 @default.
• W2319345553 cites W1996884976 @default.
• W2319345553 cites W2001564659 @default.
• W2319345553 cites W2003548212 @default.
• W2319345553 cites W2004522121 @default.
• W2319345553 cites W2004659474 @default.
• W2319345553 cites W2005705806 @default.
• W2319345553 cites W2005755533 @default.
• W2319345553 cites W2007499410 @default.
• W2319345553 cites W2007880623 @default.
• W2319345553 cites W2008619793 @default.
• W2319345553 cites W2009165342 @default.
• W2319345553 cites W2009168970 @default.
• W2319345553 cites W2009497794 @default.
• W2319345553 cites W2009628603 @default.
• W2319345553 cites W2010203036 @default.
• W2319345553 cites W2012528990 @default.
• W2319345553 cites W2013202400 @default.
• W2319345553 cites W2013544411 @default.
• W2319345553 cites W2015618010 @default.
• W2319345553 cites W2019427203 @default.
• W2319345553 cites W2019589994 @default.
• W2319345553 cites W2019823845 @default.
• W2319345553 cites W2019917125 @default.
• W2319345553 cites W2020019548 @default.
• W2319345553 cites W2022254674 @default.
• W2319345553 cites W2024370100 @default.
• W2319345553 cites W2027855953 @default.
• W2319345553 cites W2030383998 @default.
• W2319345553 cites W2031047943 @default.
• W2319345553 cites W2032276585 @default.
• W2319345553 cites W2032576629 @default.
• W2319345553 cites W2036215348 @default.
• W2319345553 cites W2037876980 @default.
• W2319345553 cites W2041302454 @default.
• W2319345553 cites W2045516356 @default.
• W2319345553 cites W2046388159 @default.
• W2319345553 cites W2049100226 @default.
• W2319345553 cites W2049156824 @default.
• W2319345553 cites W2049203104 @default.
• W2319345553 cites W2052688542 @default.
• W2319345553 cites W2053776269 @default.
• W2319345553 cites W2053907218 @default.
• W2319345553 cites W2054627147 @default.
• W2319345553 cites W2056350144 @default.
• W2319345553 cites W2058976564 @default.
• W2319345553 cites W2060034277 @default.
• W2319345553 cites W2061434022 @default.
• W2319345553 cites W2063184182 @default.
• W2319345553 cites W2064094137 @default.
• W2319345553 cites W2066384900 @default.

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