Figure 6.

Schema of negative crosstalk between TRPC6 and TRPC3-Nox2 complex in cardiomyocytes. In resting condition, TRPC3 and TRPC6 channels function independently or coordinately in cardiomyocytes. Once hearts are exposed to environmental stresses such as hemodynamic load and hyperglycemia, TRPC3 forms stable protein complex with Nox2, which evokes aberrant ROS production in cardiomyocytes. In contrast, environmental stresses also upregulate TRPC6, which can counteract formation of the TRPC3-Nox2 complex in cardiomyocytes, leading to Nox2 destabilization, and resulting in negative regulation of ROS signaling in heart.