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dc.creatorAndrades, Michael Everton
dc.creatorMorina, Arian
dc.creatorSpasić, Snežana
dc.creatorSpasojević, Ivan
dc.date.accessioned2019-01-30T17:26:28Z
dc.date.available2019-01-30T17:26:28Z
dc.date.issued2011
dc.identifier.issn1466-609X
dc.identifier.urihttp://cer.ihtm.bg.ac.rs/handle/123456789/822
dc.description.abstractThe pathogenesis of sepsis and its progression to multiple organ dysfunction syndrome and septic shock have been the subject of investigations for nearly half a century. Controversies still exist with regard to understanding the molecular pathophysiology of sepsis in relation to the complex roles played by reactive oxygen species, nitric oxide, complements and cytokines. In the present review we categorise the key turning points in sepsis development and outline the most probable sequence of events leading to cellular dysfunction and organ failure under septic conditions. We have applied an integrative approach in order to fuse current state-of-the-art knowledge about redox processes involving hydrogen peroxide, nitric oxide, superoxide, peroxynitrite and hydroxyl radical, which lead to mitochondrial respiratory dysfunction. Finally, from this point of view, the potential of redox therapy targeting sepsis is discussed.en
dc.publisherBiomed Central Ltd, London
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173014/RS//
dc.relationinfo:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/43004/RS//
dc.rightsopenAccess
dc.sourceCritical Care
dc.titleBench-to-bedside review: Sepsis - from the redox point of viewen
dc.typearticle
dc.rights.licenseARR
dcterms.abstractAндрадес, Мицхаел Евертон; Морина, Aриан; Спасојевиц, Иван; Спасић, Снежана;
dc.citation.volume15
dc.citation.issue5
dc.citation.other15(5):
dc.citation.rankM21
dc.identifier.pmid21996422
dc.identifier.doi10.1186/cc10334
dc.identifier.rcubConv_2784
dc.identifier.fulltexthttp://cer.ihtm.bg.ac.rs//bitstream/id/9422/820.pdf
dc.identifier.scopus2-s2.0-80054678294
dc.identifier.wos000303048200073
dc.type.versionpublishedVersion


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