Endothelial peroxisomal dysfunction and impaired pexophagy promotes oxidative damage in lipopolysaccharide-induced acute kidney injury.

Citation data:

Antioxidants & redox signaling, ISSN: 1557-7716, Vol: 19, Issue: 3, Page: 211-30

Publication Year:
2013
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PMID:
23088293
DOI:
10.1089/ars.2012.4768
PMCID:
PMC3691927
Author(s):
Vasko, Radovan; Ratliff, Brian B; Bohr, Stefan; Nadel, Ellen; Chen, Jun; Xavier, Sandhya; Chander, Praveen; Goligorsky, Michael S
Publisher(s):
Mary Ann Liebert Inc
Tags:
Biochemistry, Genetics and Molecular Biology
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article description
We examined that (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 (LPS), and (c) the mechanisms of peroxisomal contribution to renal injury. To accomplish this, we used lysosome-defective Lyst-mice in vivo and primary endothelial cells in vitro, and compared the responses with wild-type (WT) littermates.