Reduction of oxidative stress during recovery accelerates normalization of primary cilia length that is altered after ischemic injury in murine kidneys

American Journal of Physiology - Renal Physiology

Volumn 304, Issue 10, 2013, Pages 1283-1294

  Kim, Jee In ^a   Kim, Jinu ^a   Jang, Hee Seong ^a   Noh, Mi Ra ^a   Lipschutz, Joshua H ^b   Park, Kwon Moo ^a  

^a Kyungpook National University School of Medicine   (South Korea)

^b UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

ERK; Ischemia; Primary cilia; Reactive oxygen species; ROS

Indexed keywords

1,4 DIAMINO 1,4 BIS(2 AMINOPHENYLTHIO) 2,3 DICYANOBUTADIENE; ANTIOXIDANT; CREATININE; HYDROGEN PEROXIDE; MANGANESE TETRAKIS (1 METHYL 4 PYRIDYL) PORPHYRIN; REACTIVE OXYGEN METABOLITE; TUBULIN; UNCLASSIFIED DRUG;

ACETYLATION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL DAMAGE; CELL DIFFERENTIATION; CELL ELONGATION; CELL MATURATION; CELL PROLIFERATION; CELL REGENERATION; CELL SIZE; CONTROLLED STUDY; CONVALESCENCE; CREATININE BLOOD LEVEL; HISTOPATHOLOGY; KIDNEY ISCHEMIA; KIDNEY TUBULE CELL; MALE; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIMARY CILIUM; PRIORITY JOURNAL; PROTEIN URINE LEVEL; REPERFUSION INJURY;

EID: 84878652905     PISSN: 1931857X     EISSN: 15221466     Source Type: Journal    
DOI: 10.1152/ajprenal.00427.2012     Document Type: Article

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