Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models

The mechanism of mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, remains largely unknown. Here, we have demonstrated a striking morphological change of mitochondria in experimental models of renal ischemia/reperfusion and cisplatin-induced nephrotoxici...

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Veröffentlicht in:	The Journal of clinical investigation 2009-05, Vol.119 (5), p.1275-1285
Hauptverfasser:	Brooks, Craig, Wei, Qingqing, Cho, Sung-Gyu, Dong, Zheng
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenosine Triphosphate - deficiency Animals Apoptosis Apoptosis - drug effects Biomedical research Caspase Inhibitors Cell culture Cell death Cell Line Cells, Cultured Cisplatin - pharmacology Complications and side effects Cytochrome Cytochromes c - metabolism Drug therapy Dynamins - genetics Dynamins - metabolism Enzyme Inhibitors - pharmacology Enzyme Inhibitors - therapeutic use GTP Phosphohydrolases - antagonists & inhibitors GTP Phosphohydrolases - genetics Imaging, Three-Dimensional Ischemia Kidney diseases Kidney Tubular Necrosis, Acute - chemically induced Kidney Tubular Necrosis, Acute - pathology Kidney Tubular Necrosis, Acute - prevention & control Kidney Tubules, Proximal - cytology Kidneys Male Management Mice Mice, Inbred C57BL Microtubule-Associated Proteins - antagonists & inhibitors Microtubule-Associated Proteins - genetics Mitochondria Mitochondria - metabolism Mitochondria - pathology Mitochondria - ultrastructure Mitochondrial diseases Morphology Physiological aspects Proteins Proto-Oncogene Proteins c-bcl-2 - genetics Rats Reperfusion Injury - pathology Reperfusion Injury - prevention & control Risk factors RNA, Small Interfering - genetics Sodium Azide - pharmacology
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