UCP2-induced hypoxia promotes lipid accumulation and tubulointerstitial fibrosis during ischemic kidney injury

Mitochondrial dysfunction leads to loss of renal function and structure; however, the precise mechanisms by which mitochondrial function can regulate renal fibrosis remain unclear. Proximal tubular cells (PTCs) prefer fatty acid oxidation as their energy source and dysregulation of lipid metabolism...

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Veröffentlicht in:	Cell death & disease 2020-01, Vol.11 (1), p.26-26, Article 26
Hauptverfasser:	Ke, Qingqing, Yuan, Qi, Qin, Nan, Shi, Caifeng, Luo, Jing, Fang, Yi, Xu, Lingling, Sun, Qi, Zen, Ke, Jiang, Lei, Zhou, Yang, Yang, Junwei
Format:	Artikel
Sprache:	eng
Schlagworte:	13/1 13/109 13/51 14/19 14/63 42/89 631/80/304 64/60 692/699/1585/104/1586 82/29 82/80 9/10 Animals Antibodies Biochemistry Biomedical and Life Sciences Biopsy Cell Biology Cell Culture Cell Respiration Cells, Cultured Collagen (type I) Extracellular matrix Extracellular Matrix - metabolism Fibronectin Fibrosis Humans Hypoxia Hypoxia - metabolism Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Hypoxia-inducible factors Immunology Ischemia Ischemia - metabolism Kidney - injuries Kidney - pathology Kidney Diseases - metabolism Kidney Diseases - pathology Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - pathology Kidneys Life Sciences Lipid Metabolism Lipids Male Metabolism Mice, Inbred C57BL Mitochondria Mitochondria - metabolism Mitochondrial uncoupling protein 2 Oxidation Oxygen - metabolism Protective Agents - metabolism Renal function Reperfusion Injury - pathology siRNA Structure-function relationships Therapeutic applications Uncoupling Protein 2 - deficiency Uncoupling Protein 2 - metabolism
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