Kidney ischaemia is associated with a loss of intracellular potassium and an increase in intracellular levels of sodium, chloride and calcium; however, the mechanisms involved in the loss of cellular ion homeostasis are unknown. A new study has revealed a critical role for the nonselective cation channel TRPM2 in promoting acute kidney injury (AKI) via a mechanism that involves the activation of RAC1, oxidative stress and mitochondrial apoptotic pathways. The researchers believe that targeting TRPM2 or RAC1 might be a strategy to reduce or prevent ischaemic AKI.
References
Gao, G. et al. TRPM2 mediates ischemic kidney injury and oxidant stress through RAC1. J. Clin. Invest. 10.1172/JCI76042
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TRPM2 and RAC1: mediators of oxidative stress in AKI. Nat Rev Nephrol 10, 674 (2014). https://doi.org/10.1038/nrneph.2014.206
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DOI: https://doi.org/10.1038/nrneph.2014.206