Fig. 4

The role of CHI3L1 in ischemic stroke progression. The absence of CHI3L1 accelerates stroke progression, as observed in CHI3L1 knockout models. In these models, there was an increased release of proinflammatory cytokines such as IL-6 and IL-1β, along with a decreased release of anti-inflammatory cytokines like IL-10 and IL-4. Additionally, there was heightened expression of inflammation-related proteins, including iNOS, COX-2, Iba-1, and GFAP. As a result, the deletion of CHI3L1 exacerbates neuroinflammation and neuronal cell death following ischemia, further accelerating stroke progression