The role of immune cells glycolysis in neuroinflammation secondary to intracerebral hemorrhage

Abstract

Intracerebral hemorrhage (ICH) is the most lethal subtype of stroke, making the effective prevention and treatment of inflammatory secondary injury crucial. Recently, the role of immune cell metabolism in ICH has gained attention, particularly the regulatory mechanisms of glycolytic reprogramming in neuroinflammation. This review explores how glycolysis activation in peripheral immune cells (including neutrophils, macrophages, T cells, and natural killer cells), central immune cells (microglia), and other glial cells (including astrocytes and oligodendrocytes) involved in immune regulation influences the inflammatory response following ICH. We analyze the metabolic shifts in glycolysis within these immune cells, highlighting its dual role in neuroinflammation: glycolysis not only provides rapid energy to immune cells, which can either promote or inhibit inflammation, but lactate—a glycolysis byproduct—can modulate inflammatory damage by altering pH and immune cell function. Furthermore, we explore the therapeutic potential of targeting glycolysis in immune cells for neuroinflammation treatment. A deeper understanding of the glycolytic mechanism in ICH may facilitate the development of clinical therapeutic strategies targeting metabolism.