Klotho deficiency aggravates sepsis-related multiple organ dysfunction

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorJORGE, Lecticia B.
dc.contributor.authorCOELHO, Fernanda O.
dc.contributor.authorSANCHES, Talita R.
dc.contributor.authorMALHEIROS, Denise M. A. C.
dc.contributor.authorSOUZA, Leandro Ezaquiel de
dc.contributor.authorSANTOS, Fernando dos
dc.contributor.authorLIMA, Larissa de Sa
dc.contributor.authorSCAVONE, Cristoforo
dc.contributor.authorIRIGOYEN, Maria
dc.contributor.authorKURO-O, Makoto
dc.contributor.authorANDRADE, Lucia
dc.date.accessioned2019-05-30T13:38:46Z
dc.date.available2019-05-30T13:38:46Z
dc.date.issued2019
dc.description.abstractSepsis-induced organ failure is characterized by a massive inflammatory response and oxidative stress. Acute kidney injury (AKI) occurs in approximately half of patients in septic shock, and the mortality associated with sepsis-induced AKI is unacceptably high. Klotho is a protein expressed by renal cells and has anti-senescence properties. Klotho has also been shown to protect the kidneys in ischemia-reperfusion injury and to have antioxidant properties. To analyze the role of Klotho in sepsis-related organ dysfunction and AKI, we used a cecal ligation and puncture (CLP) model of sepsis in heterozygous Klotho-haploinsufficient mice and their wild-type littermates (CLP-Kl/+ and CLP-WT mice, respectively). In comparison with the CLP-WT mice, CLP-Kl/+ mice showed lower survival, impaired renal function, impaired hepatic function, greater oxidative stress, upregulation of inflammatory pathways (at the systemic and kidney tissue levels), and increased NF-KB activation. It is noteworthy that CLP-Kl/+ mice also showed lower heart-rate variability, less sympathetic activity, impaired baroreflex sensitivity to sodium nitroprussidc, and a blunted blood pressure response to phenylephrine. We also demonstrated that sepsis creates a state of acute Klotho deficiency. Given that low Klotho expression exacerbates sepsis and multiple organ dysfunction. Klotho might play a protective role in sepsis, especially in elderly individuals in whom Klotho expression is naturally reduced.eng
dc.description.indexMEDLINEeng
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP
dc.description.sponsorshipSao Paulo Research Foundation) [2010/08529-2, 2010/19012-0]
dc.description.sponsorshipBrazilian Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq
dc.description.sponsorshipNational Council for Scientific and Technological Development) [141496/2014-2, 301193/2016-9]
dc.description.sponsorshipFAPESP [2012/03025-1]
dc.identifier.citationAMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, v.316, n.3, p.F438-F448, 2019
dc.identifier.doi10.1152/ajprenal.00625.2017
dc.identifier.eissn1522-1466
dc.identifier.issn1931-857X
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/31828
dc.language.isoeng
dc.publisherAMER PHYSIOLOGICAL SOCeng
dc.relation.ispartofAmerican Journal of Physiology-Renal Physiology
dc.rightsrestrictedAccesseng
dc.rights.holderCopyright AMER PHYSIOLOGICAL SOCeng
dc.subjectacute kidney injuryeng
dc.subjectautonomic disordereng
dc.subjectKlothoeng
dc.subjectmultiple organ dysfunctioneng
dc.subjectsepsiseng
dc.subject.otheracute kidney injuryeng
dc.subject.othernf-kappa-beng
dc.subject.otheracute-renal-failureeng
dc.subject.othernitric-oxide synthaseeng
dc.subject.otherspectral-analysiseng
dc.subject.otheralpha-klothoeng
dc.subject.otherheart-rateeng
dc.subject.otherapoptosiseng
dc.subject.otherbiomarkereng
dc.subject.otherexpressioneng
dc.subject.wosPhysiologyeng
dc.subject.wosUrology & Nephrologyeng
dc.titleKlotho deficiency aggravates sepsis-related multiple organ dysfunctioneng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.affiliation.countryJapão
hcfmusp.affiliation.countryisojp
hcfmusp.author.externalSANTOS, Fernando dos:Univ Sao Paulo, Heart Inst, Sch Med, Sao Paulo, Brazil
hcfmusp.author.externalLIMA, Larissa de Sa:Univ Sao Paulo, Dept Pharmacol, Inst Biomed Sci, Sao Paulo, Brazil
hcfmusp.author.externalSCAVONE, Cristoforo:Univ Sao Paulo, Dept Pharmacol, Inst Biomed Sci, Sao Paulo, Brazil
hcfmusp.author.externalKURO-O, Makoto:Jichi Med Univ, Mol Med Dept, Shimotsuke, Tochigi, Japan
hcfmusp.citation.scopus21
hcfmusp.contributor.author-fmusphcLECTICIA BARBOSA JORGE
hcfmusp.contributor.author-fmusphcFERNANDA BORGES SILVA BARBOSA
hcfmusp.contributor.author-fmusphcTALITA ROJAS CUNHA SANCHES
hcfmusp.contributor.author-fmusphcDENISE MARIA AVANCINI COSTA MALHEIROS
hcfmusp.contributor.author-fmusphcLEANDRO EZIQUIEL DE SOUZA
hcfmusp.contributor.author-fmusphcMARIA CLAUDIA COSTA IRIGOYEN
hcfmusp.contributor.author-fmusphcLUCIA DA CONCEICAO ANDRADE
hcfmusp.description.beginpageF438
hcfmusp.description.endpageF448
hcfmusp.description.issue3
hcfmusp.description.volume316
hcfmusp.origemWOS
hcfmusp.origem.pubmed30516423
hcfmusp.origem.scopus2-s2.0-85061620119
hcfmusp.origem.wosWOS:000462008700004
hcfmusp.publisher.cityBETHESDAeng
hcfmusp.publisher.countryUSAeng
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