Figure 5.

Schematic representation of TRPA1-mediated myelin damage after ICH. TRPA1 is activated by the increased reactive oxygen species (ROS) after ICH, leading to an increase in the TRPA1-mediated Ca²⁺ influx. The increased Ca²⁺ further contributes to the rise in NOX1 and Calpain1, causing oxidative stress damage and myelin degradation. Axons that lose myelin protection are more susceptible to ICH injury. The damaged white matter eventually aggravates motor dysfunction in the mice.