Interleukin‑6 and ischemic stroke: From mechanisms to clinical prospects (Review)

Neuroinflammation is a central component of the pathophysiology of ischemic stroke (IS). Suppressing excessive inflammatory responses after stroke can markedly improve patient outcomes. Interleukin‑6 (IL‑6), a key mediator of the inflammatory cascade, serves a notable role in the pathological process of acute IS through multiple mechanisms. Elevated serum IL‑6 levels serve as an important biomarker for predicting the onset and recurrence of IS and are closely associated with disease severity and prognosis. Anti‑inflammatory interventions are notably important during the acute phase and secondary prevention of stroke. Currently, therapeutic strategies targeting the IL‑6/IL‑6R signaling axis are under investigation and have shown promising clinical potential. The present review summarizes the important role of IL‑6 in neuroinflammation associated with IS, its association with disease severity and prognosis and previous advances in anti‑inflammatory therapeutic strategies targeting the IL‑6/IL‑6R pathway during both the acute phase and secondary prevention of IS.