Abstract
Cerebral ischemia-reperfusion injury (CIRI), a major condition that poses a considerable threat to human health, has high incidence, disability and mortality rates. Mitigating brain damage during reperfusion has been the focal point of research due to the complex physiological and pathological changes that occur during this process. Histone lactylation has garnered considerable attention from researchers as a novel post-translational modification. Lactate, a metabolic byproduct, regulates gene transcription through histone lactylation, thereby linking cellular metabolism to gene expression programs and contributing to the development of diverse diseases. The present review comprehensively discusses the mechanisms underlying histone lactylation in CIRI and explores its potential clinical applications. The present review aims to offer an understanding of the role of lactylation in CIRI to facilitate the development of novel therapeutic strategies and drugs, and to offer novel insights and directions for the prevention and treatment of CIRI.