Mechanisms behind the beneficial effects observed with C21 induced AT2R signalling in experimental stroke have been attributed to reduced proinflammatory cytokines [262,264], reduced apoptosis [193,265,267], reduced ROS and oxidative stress [194,262,267], increased VEGF production [266], increased BDNF production [193,267], a switch from the M1 to M2 microglia phenotype [270], BBB stabilisation [194,262], and increased angiogenesis [267] (Table 2). Here, BDNF is linked to stroke disorder.