Peroxisomes and Kidney Damage

Vasko, Radovan

dc.contributor.advisor	Dihazi, Hassan Prof. Dr.
dc.contributor.author	Vasko, Radovan
dc.date.accessioned	2014-12-12T09:38:15Z
dc.date.available	2014-12-23T23:50:06Z
dc.date.issued	2014-12-12
dc.identifier.uri	http://hdl.handle.net/11858/00-1735-0000-0023-995E-C
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-4825
dc.language.iso	eng	de
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subject.ddc	610	de
dc.title	Peroxisomes and Kidney Damage	de
dc.type	doctoralThesis	de
dc.contributor.referee	Dihazi, Hassan Prof. Dr.
dc.date.examination	2014-12-16
dc.description.abstracteng	This 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.coReferee	Thumm, Michael Prof. Dr.
dc.subject.eng	peroxisomes	de
dc.subject.eng	pexophagy	de
dc.subject.eng	endotoxic stress	de
dc.subject.eng	renal damage	de
dc.identifier.urn	urn:nbn:de:gbv:7-11858/00-1735-0000-0023-995E-C-7
dc.affiliation.institute	Medizinische Fakultät	de
dc.subject.gokfull	Medizin (PPN619874732)	de
dc.subject.gokfull	Pathophysiologie {Medizin} (PPN619875305)	de
dc.description.embargoed	2014-12-23
dc.identifier.ppn	812644751

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