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Inflammasome activation by cell volume regulation and inflammation-associated hyponatremia: A vicious cycle

DC Field Value Language
dc.contributor.author신재일-
dc.contributor.author유제욱-
dc.date.accessioned2017-10-26T07:24:28Z-
dc.date.available2017-10-26T07:24:28Z-
dc.date.issued2016-
dc.identifier.issn0306-9877-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/151990-
dc.description.abstractInflammasomes are caspase-1-activating molecular platforms that produce active interleukin (IL)-1β and are implicated in various central nervous system (CNS) diseases. These multi-protein complexes can be activated by exposure of cells to low osmolality. The inflammasome nucleotide-binding and oligomerization domain-like receptor pyrin domain-containing protein 3 (NLRP3) is hereby the main sensor of cellular osmolality. IL-1β was found to stimulate the secretion of antidiuretic hormone (ADH) from the posterior pituitary gland either by action of prostaglandins or indirectly by causing the release of IL-6. Based on these findings, we hypothesize that the hyponatremia caused by a wide range of CNS diseases is able to induce significant cell swelling with induction of a hyposmotic intracellular environment, which activates the NLRP3 inflammasome, causing the release of IL-1β and induced by IL-1β, IL-6, which increases the production of ADH that leads to more profound hyponatremia. Supportive evidence for this hypothesis is the finding that IL-1 injection can induce ADH release and hyposmotic effect of ADH induced hyponatremia can, via the mechanical effect of cell swelling, activate transient receptor potential channels, which via transforming growth factor β-activated kinase 1 activate NLRP3. Implications of this hypothesis, if confirmed, would include that hyponatremia can be exacerbated through this vicious cycle but also that the inflammasomes are key mediators of this process. Confirmation of this hypothesis would have implications for prevention and clinical management of changes in patients sodium levels related to syndrome of inappropriate antidiuretic hormone secretion (SIADH) with interventions targeting inflammatory mediator production and function of inflammasomes with the potential of prevention of permanent brain damage in a wide range of CNS diseases.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherEden Press-
dc.relation.isPartOfMEDICAL HYPOTHESES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCell Size*-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCentral Nervous System/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHHyponatremia/metabolism-
dc.subject.MESHHyponatremia/physiopathology*-
dc.subject.MESHInappropriate ADH Syndrome/metabolism-
dc.subject.MESHInappropriate ADH Syndrome/physiopathology-
dc.subject.MESHInflammasomes/metabolism*-
dc.subject.MESHInflammation-
dc.subject.MESHInterleukin-1beta/metabolism-
dc.subject.MESHInterleukin-6/metabolism-
dc.subject.MESHLysosomes/metabolism-
dc.subject.MESHMice-
dc.subject.MESHModels, Theoretical-
dc.subject.MESHNLR Family, Pyrin Domain-Containing 3 Protein/metabolism-
dc.subject.MESHNeurons/pathology-
dc.subject.MESHOsmolar Concentration-
dc.subject.MESHOsmosis-
dc.subject.MESHRats-
dc.subject.MESHRats, Wistar-
dc.subject.MESHStress, Mechanical-
dc.titleInflammasome activation by cell volume regulation and inflammation-associated hyponatremia: A vicious cycle-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Pediatrics-
dc.contributor.googleauthorJ.H. Kim-
dc.contributor.googleauthorJ.H. Park-
dc.contributor.googleauthorM. Eisenhut-
dc.contributor.googleauthorJ.W. Yu-
dc.contributor.googleauthorJ.I. Shin-
dc.identifier.doi10.1016/j.mehy.2016.05.018-
dc.contributor.localIdA02508-
dc.contributor.localIdA02142-
dc.relation.journalcodeJ02200-
dc.identifier.eissn1532-2777-
dc.identifier.pmid27372869-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0306987716301414?via%3Dihub-
dc.contributor.alternativeNameShin, Jae Il-
dc.contributor.alternativeNameYu, Je Wook-
dc.contributor.affiliatedAuthorYu, Je Wook-
dc.contributor.affiliatedAuthorShin, Jae Il-
dc.citation.volume93-
dc.citation.startPage117-
dc.citation.endPage121-
dc.identifier.bibliographicCitationMEDICAL HYPOTHESES, Vol.93 : 117-121, 2016-
dc.date.modified2017-10-24-
dc.identifier.rimsid46312-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아과학교실) > 1. Journal Papers

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