Ischemic stroke (IS) accounts for ~85% of all stroke cases and stands as one of the leading global causes of disability and mortality. Its pathological progression is closely intertwined with intricate inflammatory responses, among which post-stroke activated macrophages are widely recognized as the core drivers and regulators of IS pathogenesis. This review systematically elucidates the dual role of macrophages in stroke: they act as the primary drivers of the acute neuroinflammatory storm, while also serving as key regulators of neurorepair during the subacute and chronic phases. By focusing on the spatiotemporal dynamic changes, polarization regulatory mechanisms, and phenotypic/functional transition patterns of macrophages. This review provides a theoretical foundation for the development of precise therapeutic strategies that target the spatiotemporal dynamics and functional transitions of macrophages.
Zhang et al. (2026) studied this question.