Figure 10.

The proposed mechanism of TRPA1 activation in renal tubular epithelial cells by hypoxia-reoxygenation (H/R) or I/R for the induction of renal inflammation and renal injury. As shown, H/R or I/R causes ROS increase, which in turn activates renal epithelial TRPA1, thereby, ultimately promoting of Ca²⁺ influx. The increase of intracellular Ca²⁺ in renal epithelial cells then contributes to the activation of NADPH oxidase, which can result in the elevation of the intracellular ROS. This effect activates the MAPKs/NF-κB signaling pathway, which allows the induction of inflammatory chemokines and aggravates renal injury.