PMC:7373848 / 20232-22452 JSON TXT

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LitCovid_Glycan-Motif-Structure

{"project":"LitCovid_Glycan-Motif-Structure","denotations":[{"id":"T3","span":{"begin":824,"end":834},"obj":"https://glytoucan.org/Structures/Glycans/G00017MO"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T94","span":{"begin":1197,"end":1202},"obj":"Body_part"},{"id":"T95","span":{"begin":1329,"end":1335},"obj":"Body_part"},{"id":"T96","span":{"begin":1631,"end":1642},"obj":"Body_part"},{"id":"T97","span":{"begin":1830,"end":1836},"obj":"Body_part"},{"id":"T98","span":{"begin":2155,"end":2159},"obj":"Body_part"}],"attributes":[{"id":"A94","pred":"uberon_id","subj":"T94","obj":"http://purl.obolibrary.org/obo/UBERON_0000062"},{"id":"A95","pred":"uberon_id","subj":"T95","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A96","pred":"uberon_id","subj":"T96","obj":"http://purl.obolibrary.org/obo/UBERON_0001986"},{"id":"A97","pred":"uberon_id","subj":"T97","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A98","pred":"uberon_id","subj":"T98","obj":"http://purl.obolibrary.org/obo/UBERON_0012245"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

LitCovid-PubTator

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T73","span":{"begin":32,"end":38},"obj":"Disease"},{"id":"T74","span":{"begin":385,"end":391},"obj":"Disease"},{"id":"T75","span":{"begin":875,"end":881},"obj":"Disease"},{"id":"T76","span":{"begin":932,"end":941},"obj":"Disease"},{"id":"T77","span":{"begin":943,"end":948},"obj":"Disease"},{"id":"T78","span":{"begin":1026,"end":1032},"obj":"Disease"},{"id":"T79","span":{"begin":1189,"end":1196},"obj":"Disease"},{"id":"T80","span":{"begin":1203,"end":1209},"obj":"Disease"},{"id":"T81","span":{"begin":1837,"end":1843},"obj":"Disease"},{"id":"T82","span":{"begin":1855,"end":1867},"obj":"Disease"}],"attributes":[{"id":"A73","pred":"mondo_id","subj":"T73","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A74","pred":"mondo_id","subj":"T74","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A75","pred":"mondo_id","subj":"T75","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A76","pred":"mondo_id","subj":"T76","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A77","pred":"mondo_id","subj":"T77","obj":"http://purl.obolibrary.org/obo/MONDO_0005070"},{"id":"A78","pred":"mondo_id","subj":"T78","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A79","pred":"mondo_id","subj":"T79","obj":"http://purl.obolibrary.org/obo/MONDO_0005047"},{"id":"A80","pred":"mondo_id","subj":"T80","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A81","pred":"mondo_id","subj":"T81","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A82","pred":"mondo_id","subj":"T82","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T22","span":{"begin":943,"end":948},"obj":"Phenotype"},{"id":"T23","span":{"begin":1845,"end":1850},"obj":"Phenotype"}],"attributes":[{"id":"A22","pred":"hp_id","subj":"T22","obj":"http://purl.obolibrary.org/obo/HP_0002664"},{"id":"A23","pred":"hp_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/HP_0000969"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T87","span":{"begin":767,"end":778},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T88","span":{"begin":949,"end":957},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T89","span":{"begin":949,"end":957},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T90","span":{"begin":949,"end":957},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T91","span":{"begin":949,"end":957},"obj":"http://purl.obolibrary.org/obo/GO_0001906"},{"id":"T92","span":{"begin":1082,"end":1092},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T93","span":{"begin":1131,"end":1141},"obj":"http://purl.obolibrary.org/obo/GO_0070269"},{"id":"T94","span":{"begin":1267,"end":1277},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T95","span":{"begin":1562,"end":1575},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T96","span":{"begin":1779,"end":1808},"obj":"http://purl.obolibrary.org/obo/GO_0050820"},{"id":"T97","span":{"begin":1797,"end":1808},"obj":"http://purl.obolibrary.org/obo/GO_0050817"},{"id":"T98","span":{"begin":1855,"end":1867},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T99","span":{"begin":2169,"end":2179},"obj":"http://purl.obolibrary.org/obo/GO_0008219"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

LitCovid-PD-GlycoEpitope

{"project":"LitCovid-PD-GlycoEpitope","denotations":[{"id":"T4","span":{"begin":803,"end":818},"obj":"GlycoEpitope"}],"attributes":[{"id":"A4","pred":"glyco_epitope_db_id","subj":"T4","obj":"http://www.glycoepitope.jp/epitopes/EP0086"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T140","span":{"begin":0,"end":38},"obj":"Sentence"},{"id":"T141","span":{"begin":39,"end":105},"obj":"Sentence"},{"id":"T142","span":{"begin":106,"end":225},"obj":"Sentence"},{"id":"T143","span":{"begin":226,"end":322},"obj":"Sentence"},{"id":"T144","span":{"begin":323,"end":413},"obj":"Sentence"},{"id":"T145","span":{"begin":414,"end":535},"obj":"Sentence"},{"id":"T146","span":{"begin":536,"end":840},"obj":"Sentence"},{"id":"T147","span":{"begin":841,"end":942},"obj":"Sentence"},{"id":"T148","span":{"begin":943,"end":1004},"obj":"Sentence"},{"id":"T149","span":{"begin":1005,"end":1167},"obj":"Sentence"},{"id":"T150","span":{"begin":1168,"end":1210},"obj":"Sentence"},{"id":"T151","span":{"begin":1211,"end":1410},"obj":"Sentence"},{"id":"T152","span":{"begin":1411,"end":1606},"obj":"Sentence"},{"id":"T153","span":{"begin":1607,"end":1668},"obj":"Sentence"},{"id":"T154","span":{"begin":1669,"end":1762},"obj":"Sentence"},{"id":"T155","span":{"begin":1763,"end":1868},"obj":"Sentence"},{"id":"T156","span":{"begin":1869,"end":1956},"obj":"Sentence"},{"id":"T157","span":{"begin":1957,"end":2148},"obj":"Sentence"},{"id":"T158","span":{"begin":2149,"end":2168},"obj":"Sentence"},{"id":"T159","span":{"begin":2169,"end":2203},"obj":"Sentence"},{"id":"T160","span":{"begin":2204,"end":2220},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

LitCovid-PMC-OGER-BB

2_test

{"project":"2_test","denotations":[{"id":"32700024-31454337-64991481","span":{"begin":409,"end":411},"obj":"31454337"},{"id":"32700024-28885470-64991482","span":{"begin":621,"end":623},"obj":"28885470"},{"id":"32700024-28885470-64991483","span":{"begin":836,"end":838},"obj":"28885470"},{"id":"32700024-3458948-64991484","span":{"begin":1000,"end":1002},"obj":"3458948"}],"text":"Histones cause endothelial cell injury\nFive major families of histones exist: H1/H5, H2A, H2B, H3 and H4. Histones H2A, H2B, H3 and H4 are known as the core histones, while histones H1 and H5 are known as the linker histones. The core histones are dimers and all possess the histone fold domain (reviewed in Simpson) [45].\nExtracellular histones are cytoxic and cause endothelial cell injury and dysfunction [46]. The cytotoxicity primarily occurs within the microcirculatory system, and causes ultrastructural changes and dysfunction. Altered flow dynamics cause further endothelial cell damage and glycocalyx shedding [47] Inflammatory conditions with high concentrations of extracellular histones and cytokines damage the endothelial glycocalyx accompanied by its degradation shedding of syndecan-1, heparan sulfate, and hyaluronan [47].\nCytokine-induced endothelial cell injury occurs in a variety of conditions including acute infection. Tumor necrosis factor (TNF)-α is particularly cytotoxic [48]. The mechanism(s) for injury include recruitment and binding of monocytes, up-regulation of caspase-1, IL-1β and expression of pyroptosis-related factors (Fig. 6).\nFig. 6 Mechanisms of Sterile Organ Injury. Toxic insults initiate both controlled and uncontrolled cell death in endothelial cells leading to apoptotic/necrotic tissue and release of intracellular cell components into the extracellular space. These include immunogenic compounds such as RNA and DAMPs (HMGB1, ATP and Histone) which bind to and activate specific TLRs, driving the NFkB-mediated transcription of pro-inflammatory cytokines. Platelets adhere to the endothelium via ICAM-1 and Kindlin-3. Activated platelets release Poly P, which activates Factor XII, and subsequently, complement. This results in activation of the coagulation pathways and further tissue injury, edema and inflammation. Activated T cells release pro-inflammatory mediators and can cause direct cytotoxicity. High mobility group box (HMGB)-1, damage associated molecular patterns (DAMPS), toll-like receptors (TLR), reactive oxygen species (ROS), polyphosphates (Poly-P), adenosine triphosphate (ATP)\n(From Silk E et al. Cell Death Disease 2017; 8: e2812. With permission)"}

PMC:7373848 / 20232-22452 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7373848 / 20232-22452 JSON TXT