TRPV4 and hematoma: Considering the high sensitivity of TRPV4 to mechanical stress, we propose that the rapid formation of a hematoma crushes the surrounding cells and dramatically activates the Ca2+-permeable TRPV4 channel; TRPV4 activation induces Ca2+ entry and activates the Ca2+-dependent PKCα/RhoA/MLC2 pathway, thereby leading to the formation of stress fibers and disruption of the BBB during ICH.