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      Apoptosis and acute kidney injury.

      1 ,
      Kidney international
      Springer Science and Business Media LLC

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          Abstract

          Improved mechanistic understanding of renal cell death in acute kidney injury (AKI) has generated new therapeutic targets. Clearly, the classic lesion of acute tubular necrosis is not adequate to describe the consequences of renal ischemia, nephrotoxin exposure, or sepsis on glomerular filtration rate. Experimental evidence supports a pathogenic role for apoptosis in AKI. Interestingly, proximal tubule epithelial cells are highly susceptible to apoptosis, and injury at this site contributes to organ failure. During apoptosis, well-orchestrated events converge at the mitochondrion, the organelle that integrates life and death signals generated by the BCL2 (B-cell lymphoma 2) protein family. Death requires the 'perfect storm' for outer mitochondrial membrane injury to release its cellular 'executioners'. The complexity of this process affords new targets for effective interventions, both before and after renal insults. Inhibiting apoptosis appears to be critical, because circulating factors released by the injured kidney induce apoptosis and inflammation in distant organs including the heart, lung, liver, and brain, potentially contributing to the high morbidity and mortality associated with AKI. Manipulation of known stress kinases upstream of mitochondrial injury, induction of endogenous, anti-apoptotic proteins, and improved understanding of the timing and consequences of renal cell apoptosis will inevitably improve the outcome of human AKI.

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          Author and article information

          Journal
          Kidney Int
          Kidney international
          Springer Science and Business Media LLC
          1523-1755
          0085-2538
          Jul 2011
          : 80
          : 1
          Affiliations
          [1 ] Renal Section, Department of Medicine, Boston University, Boston, Massachusetts 02118, USA.
          Article
          S0085-2538(15)54927-2 NIHMS455784
          10.1038/ki.2011.120
          4625984
          21562469
          1489123c-edce-42d1-ba16-deed8941ba4a
          History

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