2019
DOI: 10.1016/bs.acc.2019.03.005
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Pentraxin-3 and endothelial dysfunction

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Cited by 61 publications
(48 citation statements)
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“…PTX-3 is produced in response to proinflammatory signals and microbial stimulation and by a wide variety of immune and endothelial cells with roles in the regulation of inflammation and complement activation as well as in vascular inflammation and endothelial cell dysfunction ( 23 , 32 ). Elevated levels of PTX-3 have been found in septic shock ( 33 , 34 ), chronic kidney disease ( 35 ), stroke ( 36 ), and a variety of cardiovascular diseases ( 25 , 37 , 38 ).…”
Section: Discussionmentioning
confidence: 99%
“…PTX-3 is produced in response to proinflammatory signals and microbial stimulation and by a wide variety of immune and endothelial cells with roles in the regulation of inflammation and complement activation as well as in vascular inflammation and endothelial cell dysfunction ( 23 , 32 ). Elevated levels of PTX-3 have been found in septic shock ( 33 , 34 ), chronic kidney disease ( 35 ), stroke ( 36 ), and a variety of cardiovascular diseases ( 25 , 37 , 38 ).…”
Section: Discussionmentioning
confidence: 99%
“…As an important component of innate humoral immunity, pentraxin-3 has the ability to bind complement component C1q and then activate the classical pathway of complement [ 25 , 26 ]. Recently, many studies have showed that pentraxin-3 could modulate inflammatory cells, interact with P-selectin, reduce the nitric oxide (NO) synthesis of endothelial cells, inhibit endothelial cells proliferation and alter their functions, and finally promote vascular inflammatory response and endothelial dysfunction [ 27 , 28 ]. Therefore, the release of pentraxin-3 by neutrophil degranulation may be an important link in the immunopathological injury of HFRS, and the level of plasma pentraxin-3 may also indirectly reflect the severity of vascular endothelial injury in patients with HFRS.…”
Section: Discussionmentioning
confidence: 99%
“…As an important component of innate humoral immunity, pentraxin-3 has the ability to bind complement component C1q and then activate the classical pathway of complement [22,23]. Recently, many studies have showed that pentraxin-3 could modulate in ammatory cells, interact with P-selectin, reduce the nitric oxide (NO) synthesis of endothelial cells, inhibit endothelial cells proliferation and alter their functions, and nally promote vascular in ammatory response and endothelial dysfunction [24,25]. Therefore, the release of pentraxin-3 by neutrophil degranulation may be an important link in the immunopathological injury of HFRS, and the level of plasma pentraxin-3 may indirectly re ect the severity of vascular endothelial injury in patients with HFRS.…”
Section: Discussionmentioning
confidence: 99%