Research progress on the regulation of microglia and astrocyte functions by protein lactylation in cerebral ischemia-reperfusion injury: A review

Protein lactylation, a novel posttranslational modification, has garnered significant attention for its regulatory mechanisms in cerebral ischemia-reperfusion injury. This review highlights the critical roles of protein lactylation in regulating microglia and astrocytes functions. By modulating the activation of microglia and astrocytes, inflammatory responses, and antioxidative stress, protein lactylation plays a pivotal role in neural repair and regeneration. Following cerebral ischemia-reperfusion injury, lactylation enhances the phagocytic activity of microglia, facilitates the clearance of necrotic cells, reduces the secretion of pro-inflammatory cytokines, and thus protects neurons. In astrocytes, lactylation modification supports blood–brain barrier integrity, provides nutritional support, and regulates antioxidative enzymes, further promoting neuronal survival and functional recovery. Further investigation into the molecular mechanisms of protein lactylation, its specific roles in glial cells, the development of novel lactylation regulators, and its interactions with other posttranslational modifications will offer new insights and directions for the treatment of cerebral ischemia-reperfusion injury.