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Inflammatory Mechanisms Contributing to Endothelial Dysfunction
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<blockquote data-quote="madman" data-source="post: 206259" data-attributes="member: 13851"><p><strong>Figure 1. <u>Inflammatory activation of endothelial cells (ECs)</u>. (<u>A</u>) Stimulation of EC receptors by damage-associated molecular patterns (High mobility group box 1 (HMGB1)), inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukins (ILs)), oxidized low-density lipoproteins (oxLDL), advanced glycation end products (AGEs), and angiotensin (Ang)-II promotes nuclear factor-κB (NF-κB) signaling which results in (<u>B</u>) upregulation of adhesion molecules (vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, E-Selectin (E-S), P-Selectin (P-S)) with subsequent monocyte (MC) adhesion and subendothelial transmigration with the aid of monocyte chemoattractant protein (MCP)-1 and its receptor C-C chemokine receptor type 2 (CCR2). Monocytes proceed to differentiate into macrophages that phagocytose oxLDL to become foam cells. (<u>C</u>) Injured endothelial cells release inflammatory mediators and tissue factor (TF) further promoting inflammation and coagulation, while the release of von-Willebrand factor (vWF) from the Weibel-Palade bodies results in platelet adhesion and aggregation following the binding with platelet glycoprotein (GP)1b. NLRP3: NLR family pyrin domain containing 3, TLR: toll-like receptor, RAGE: receptor of advanced glycation end products, VSMC: vascular smooth muscle cell.</strong></p><p><strong>[ATTACH=full]16061[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 206259, member: 13851"] [B]Figure 1. [U]Inflammatory activation of endothelial cells (ECs)[/U]. ([U]A[/U]) Stimulation of EC receptors by damage-associated molecular patterns (High mobility group box 1 (HMGB1)), inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukins (ILs)), oxidized low-density lipoproteins (oxLDL), advanced glycation end products (AGEs), and angiotensin (Ang)-II promotes nuclear factor-κB (NF-κB) signaling which results in ([U]B[/U]) upregulation of adhesion molecules (vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, E-Selectin (E-S), P-Selectin (P-S)) with subsequent monocyte (MC) adhesion and subendothelial transmigration with the aid of monocyte chemoattractant protein (MCP)-1 and its receptor C-C chemokine receptor type 2 (CCR2). Monocytes proceed to differentiate into macrophages that phagocytose oxLDL to become foam cells. ([U]C[/U]) Injured endothelial cells release inflammatory mediators and tissue factor (TF) further promoting inflammation and coagulation, while the release of von-Willebrand factor (vWF) from the Weibel-Palade bodies results in platelet adhesion and aggregation following the binding with platelet glycoprotein (GP)1b. NLRP3: NLR family pyrin domain containing 3, TLR: toll-like receptor, RAGE: receptor of advanced glycation end products, VSMC: vascular smooth muscle cell. [ATTACH type="full"]16061[/ATTACH][/B] [/QUOTE]
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General Health & Fitness
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Inflammatory Mechanisms Contributing to Endothelial Dysfunction
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