Activation of endothelial TRPM2 exacerbates blood-brain barrier degradation in ischemic stroke.

In conclusion, our data reveals a novel molecular mechanism in which TRPM2 and CD36 promote the activation of each other, which exacerbates endothelial dysfunction during ischemic stroke. Our study suggests that TRPM2 in endothelial cells is a promising target for developing more effective and safer therapies for ischemic stroke.