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Peroxisomes and Kidney Damage

dc.contributor.advisorDihazi, Hassan Prof. Dr.
dc.contributor.authorVasko, Radovan
dc.date.accessioned2014-12-12T09:38:15Z
dc.date.available2014-12-23T23:50:06Z
dc.date.issued2014-12-12
dc.identifier.urihttp://hdl.handle.net/11858/00-1735-0000-0023-995E-C
dc.identifier.urihttp://dx.doi.org/10.53846/goediss-4825
dc.language.isoengde
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subject.ddc610de
dc.titlePeroxisomes and Kidney Damagede
dc.typedoctoralThesisde
dc.contributor.refereeDihazi, Hassan Prof. Dr.
dc.date.examination2014-12-16
dc.description.abstractengThis work examined (a) how the endotoxic stress affects peroxisomal function and autophagic degradation of peroxisomes-pexophagy, (b) how a superimposed dysfunction of lysosomes and pexophagy modifies responses to lipopolysaccharide, and (c) the mechanisms of peroxisomal contribution to renal injury. To accomplish this, we used lysosome-defective mice in vivo and primary endothelial cells in vitro, and compared the responses with wild-type littermates.  We demonstrated that pexophagy is a default response to endotoxic injury. However, when lysosomal dysfunction (a frequent companion of chronic diseases) is superimposed, recycling and functioning of peroxisomes are impaired, and an imbalance between hydrogen peroxide-generating β-oxidation and hydrogen peroxide-detoxifying catalase ensues, which ultimately results in peroxisomal burnout. Our data strongly suggest that pexophagy, a cellular mechanism per se, is essential in functional maintenance of peroxisomes during lipopolysaccharide exposure. Inhibition of pexophagy results in accumulation of impaired peroxisomes, redox disequilibrium, and aggravated renal damage.de
dc.contributor.coRefereeThumm, Michael Prof. Dr.
dc.subject.engperoxisomesde
dc.subject.engpexophagyde
dc.subject.engendotoxic stressde
dc.subject.engrenal damagede
dc.identifier.urnurn:nbn:de:gbv:7-11858/00-1735-0000-0023-995E-C-7
dc.affiliation.instituteMedizinische Fakultätde
dc.subject.gokfullMedizin (PPN619874732)de
dc.subject.gokfullPathophysiologie {Medizin} (PPN619875305)de
dc.description.embargoed2014-12-23
dc.identifier.ppn812644751


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