Microparticles: markers and mediators of sepsis-induced microvascular dysfunction, immunosuppression, and AKI
Sepsis is a severe and complex syndrome that lacks effective prevention or therapeutics. The effects of sepsis on the microvasculature have become an attractive area for possible new targets and therapeutics. Microparticles (MPs) are cell membrane–derived particles that can promote coagulation, infl...
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| Veröffentlicht in: | Kidney international 2015-06, Vol.87 (6), p.1100-1108 |
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| creator | Souza, Ana Carolina P. Yuen, Peter S.T. Star, Robert A. |
| description | Sepsis is a severe and complex syndrome that lacks effective prevention or therapeutics. The effects of sepsis on the microvasculature have become an attractive area for possible new targets and therapeutics. Microparticles (MPs) are cell membrane–derived particles that can promote coagulation, inflammation, and angiogenesis, and they can participate in cell-to-cell communication. MPs retain cell membrane and cytoplasmic constituents of their parental cells, including two procoagulants: phosphatidylserine and tissue factor. We highlight the role of microparticles released by endothelial and circulating cells after sepsis-induced microvascular injury, and we discuss possible mechanisms by which microparticles can contribute to endothelial dysfunction, immunosuppression, and multiorgan dysfunction—including sepsis-AKI. Once viewed as cellular byproducts, microparticles are emerging as a new class of markers and mediators in the pathogenesis of sepsis. |
| doi_str_mv | 10.1038/ki.2015.26 |
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The effects of sepsis on the microvasculature have become an attractive area for possible new targets and therapeutics. Microparticles (MPs) are cell membrane–derived particles that can promote coagulation, inflammation, and angiogenesis, and they can participate in cell-to-cell communication. MPs retain cell membrane and cytoplasmic constituents of their parental cells, including two procoagulants: phosphatidylserine and tissue factor. We highlight the role of microparticles released by endothelial and circulating cells after sepsis-induced microvascular injury, and we discuss possible mechanisms by which microparticles can contribute to endothelial dysfunction, immunosuppression, and multiorgan dysfunction—including sepsis-AKI. 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The effects of sepsis on the microvasculature have become an attractive area for possible new targets and therapeutics. Microparticles (MPs) are cell membrane–derived particles that can promote coagulation, inflammation, and angiogenesis, and they can participate in cell-to-cell communication. MPs retain cell membrane and cytoplasmic constituents of their parental cells, including two procoagulants: phosphatidylserine and tissue factor. We highlight the role of microparticles released by endothelial and circulating cells after sepsis-induced microvascular injury, and we discuss possible mechanisms by which microparticles can contribute to endothelial dysfunction, immunosuppression, and multiorgan dysfunction—including sepsis-AKI. Once viewed as cellular byproducts, microparticles are emerging as a new class of markers and mediators in the pathogenesis of sepsis.</description><subject>Acute Kidney Injury - blood</subject><subject>Acute Kidney Injury - etiology</subject><subject>biomarkers</subject><subject>Biomarkers - blood</subject><subject>Cell-Derived Microparticles - immunology</subject><subject>Cell-Derived Microparticles - metabolism</subject><subject>coagulopathy</subject><subject>endothelial dysfunction</subject><subject>Endothelium - physiopathology</subject><subject>Humans</subject><subject>Immune Tolerance</subject><subject>Microvessels</subject><subject>Multiple Organ Failure - blood</subject><subject>Oxidative Stress</subject><subject>phosphatidylserine</subject><subject>Sepsis - blood</subject><subject>Sepsis - complications</subject><subject>thrombosis</subject><subject>tissue factor</subject><subject>Vascular Diseases - blood</subject><subject>Vascular Diseases - etiology</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkU2LFDEQhoMo7rh68QdIgxcRe0w6H514EJbFj8UVL3oOmaRas9OdtElnYP-9aWddVARPoVJPvdRbL0KPCd4STOXLvd92mPBtJ-6gDeEdbUnP-V20wVjytuNUnqAHOV_hWiuK76OTjgvVKS42aProbYqzSYu3I-RXzWTSHlJuTHDNBM6bJdYqDk2GOfvc-uCKhdpb5w4m2zKa1LjrPJRgFx_Di8ZPUwkxl3lOkPPPr1Xt7MPFQ3RvMGOGRzfvKfry9s3n8_ft5ad3F-dnl63lHC8thd5y5gTdOUnZTjoFyvaUSzsAwyCZcwIcGKGEBan4MEjRO6vsjijMHaOn6PVRdy67asJCWJIZ9Zx8tXeto_H6z07w3_TXeNCMMSWxqALPbgRS_F4gL3ry2cI4mgCxZE16rEhPOq7-jwqlmFSC9xV9-hd6FUsK9RKVklT1inayUs-PVD1wzgmG270J1mvgeu_1Grju1kWf_O70Fv2VcAXYEYB674OHpLP1EGqEPoFdtIv-X7o_AGQ3uu8</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>Souza, Ana Carolina P.</creator><creator>Yuen, Peter S.T.</creator><creator>Star, Robert A.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7QL</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20150601</creationdate><title>Microparticles: markers and mediators of sepsis-induced microvascular dysfunction, immunosuppression, and AKI</title><author>Souza, Ana Carolina P. ; 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| subjects | Acute Kidney Injury - blood Acute Kidney Injury - etiology biomarkers Biomarkers - blood Cell-Derived Microparticles - immunology Cell-Derived Microparticles - metabolism coagulopathy endothelial dysfunction Endothelium - physiopathology Humans Immune Tolerance Microvessels Multiple Organ Failure - blood Oxidative Stress phosphatidylserine Sepsis - blood Sepsis - complications thrombosis tissue factor Vascular Diseases - blood Vascular Diseases - etiology |
| title | Microparticles: markers and mediators of sepsis-induced microvascular dysfunction, immunosuppression, and AKI |
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