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Microglia, as the intrinsic immune cells in the brain, are activated following ischemic stroke. Activated microglia participate in the pathological processes after stroke through polarization, autophagy, phagocytosis, pyroptosis, ferroptosis, apoptosis, and necrosis, thereby influencing the injury and repair following stroke. It has been established that polarized M1 and M2 microglia exhibit pro-inflammatory and anti-inflammatory effects, respectively. Autophagy and phagocytosis in microglia following ischemia are dynamic processes, where moderate levels promote cell survival, while excessive responses may exacerbate neurofunctional deficits following stroke. Additionally, pyroptosis and ferroptosis in microglia after ischemic stroke contribute to the release of harmful cytokines, further aggravating the damage to brain tissue due to ischemia. This article discusses the different functional states of microglia in ischemic stroke research, highlighting current research trends and gaps, and provides insights and guidance for further study of ischemic stroke. • Microglia is important in the repair of ischemic stroke. • Microglial polarization is a double-edged sword in ischemic stroke. • Microglial proper autophagy and phagocytosis contribute to functional recovery after ischemic stroke, while excessive activation may worsen the damage. • Microglial pyroptosis, ferroptosis, apoptosis and necrosis in ischemic stroke is in the preliminary stage. [ABSTRACT FROM AUTHOR]