Temporal dynamics in the precision regulation of post-ischemic stroke neuroinflammation

Neuroinflammatory response after ischemic stroke (IS) determines the degree of tissue damage and the course of disease recovery. In acute phase. injury-related molecular patterns activate Toll-like receptor 4 (TLR4) / nuclear factor kappa-B (NF-κB) and NOD-like receptor pyrin domain-containing protein 3 (NLRP3) / caspase-1 pathways to amplify inflammatory injury. In the subacute phase, the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway regulates the polarization of M1 / M2 microglia to determine the direction of repair. In the chronic phase, prolonged inflammation hinders nerve repair and adversely affects long-term outcomes. Based on these stages, anti-inflammatory drugs, multi-target agents and non-pharmacological interventions such as cell therapy and neuromodulation are continuously emerging. However, challenges such as spatio-temporal heterogeneity of inflammation, blood-brain barrier permeability and immune differences still restrict transformation. In the future, it is necessary to establish an individualized strategy guided by immune typing based on the dynamic law of inflammation to promote precise regulation.