Stroke is the largest contributor to global neurological disability-adjusted life-years, posing a huge economic and social burden to the world. Though pharmacological recanalization with recombinant tissue plasminogen activator and mechanical thrombectomy have greatly improved the prognosis of patients with ischemic stroke, clinically, there is still no effective treatment for the secondary injury caused by cerebral ischemia. In recent years, more and more evidences show that neuroinflammation plays a pivotal role in the pathogenesis and progression of ischemic cerebral injury. Microglia are brain resident innate immune cells and act the role peripheral macrophages. They play critical roles in mediating neuroinflammation after ischemic stroke. Microglia-mediated neuroinflammation is not an isolated process and has complex relationships with other pathophysiological processes as oxidative/nitrative stress, excitotoxicity, necrosis, apoptosis, pyroptosis, autophagy, and adaptive immune response. Upon activation, microglia differentially express various receptors, channel proteins, and enzymes involved in promoting or inhibiting the inflammatory processes, making them the targets of intervention for ischemic stroke. To inhibit microglia-related neuroinflammation and promote neurological recovery after ischemic stroke, numerous biochemical agents, cellular therapies, and physical methods have been demonstrated to have therapeutic potentials. Though accumulating experimental evidences have demonstrated that targeting microglia is a promising approach in the treatment of ischemic stroke, the clinical progress is slow. Till now, no clinical study could provide convincing evidence that any biochemical or physical therapies could exert neuroprotective effect by specifically targeting microglia following ischemic stroke.

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PubMed