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Acute kidney injury

AIMing to enhance debris clearance and improve outcomes in AKI

Nature Reviews Nephrology volume 12, page 123 (2016)Cite this article

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The restoration of tubular structure and renal function after AKI requires the proliferation of surviving epithelial cells and the efficient removal of debris from dead TECs. In the injured kidney, apoptotic and necrotic TECs are phagocytosed by neighbouring injured epithelial cells, which differentiate into a phagocytic phenotype under the control of KIM-1. The importance of this phagocytic process in regeneration and recovery was demonstrated by a study in which mice expressing a mutant form of Kim-1 that lacked the ability to engulf cell debris had more severe kidney injury than mice expressing wild-type Kim-1. “The known role of phagocytosis in AKI and our previous research showing that AIM accumulates at liver cancer cells and induces their elimination led us to hypothesize that AIM might be a sort of signalling molecule that accumulates on undesired biological garbage and induces its clearance,” says Miyazaki. “In this respect we thought that AIM might attach to the intratubular dead-cell debris and induce its clearance during AKI.”

KIM-1 recognizes and binds to AIM on debris, incorporating AIM together with the debris into the TECs

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References

  1. Arai, S. et al. Apoptosis inhibitor of macrophage protein enhances intraluminal debris clearance and ameliorates acute kidney injury in mice. Nat. Med. http://dx.doi.org/10.1038/nm.4012

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  1. Susan J. Allison
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Allison, S. AIMing to enhance debris clearance and improve outcomes in AKI. Nat Rev Nephrol 12, 123 (2016). https://doi.org/10.1038/nrneph.2016.3

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