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10.1038/s41598-017-10336-8

http://scihub22266oqcxt.onion/10.1038/s41598-017-10336-8
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suck abstract from ncbi


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pmid28842716
      Sci+Rep 2017 ; 7 (1 ): 9503
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  • Pharmacological Inhibition of PTEN Aggravates Acute Kidney Injury #MMPMID28842716
  • Zhou J ; Jia L ; Hu Z ; Wang Y
  • Sci Rep 2017[Aug]; 7 (1 ): 9503 PMID28842716 show ga
  • Renal ischemia/reperfusion is a major cause of acute kidney injury. However, the pathogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully defined. Here, we investigated the role of PTEN, a dual protein/lipid phosphatase, in the development of ischemic AKI in mice. Pharmacological inhibition of PTEN with bpV(HOpic) exacerbated renal dysfunction and promoted tubular damage in mice with IRI compared with vehicle-treated mice with IRI. PTEN inhibition enhanced tubular cell apoptosis in kidneys with IRI, which was associated with excessive caspase-3 activation. Furthermore, PTEN inhibition expanded the infiltration of neutrophils and macrophages into kidneys with IRI, which was accompanied by increased expression of the proinflammatory molecules. These results have demonstrated that PTEN plays a crucial role in the pathogenesis of ischemic acute kidney injury through regulating tubular cell apoptosis and inflammation suggesting PTEN could be a potential therapeutic target for acute kidney injury.
  • |*Protein Aggregation, Pathological/complications/metabolism [MESH]
  • |Acute Kidney Injury/drug therapy/*etiology/*metabolism/physiopathology [MESH]
  • |Animals [MESH]
  • |Apoptosis/drug effects [MESH]
  • |Biomarkers [MESH]
  • |Cytokines/metabolism [MESH]
  • |Enzyme Activation [MESH]
  • |Enzyme Inhibitors/*pharmacology [MESH]
  • |Immunohistochemistry [MESH]
  • |Inflammation Mediators/metabolism [MESH]
  • |Ischemia/complications/metabolism [MESH]
  • |Male [MESH]
  • |Mice [MESH]
  • |PTEN Phosphohydrolase/*antagonists & inhibitors/*metabolism [MESH]
  • |Protein Aggregates/*drug effects [MESH]


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