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已发表论文
组蛋白乳酰化作为阿尔茨海默病病理生理学中的表观遗传调节因子：综述性评论
Authors Tang J, Zhang Y, Wang Y, Fu Y, Qi J, Xiang A, Zhao R, Tan G, Deng H, Zhou X , Wu L
Received 29 July 2025
Accepted for publication 11 October 2025
Published 11 November 2025 Volume 2025:18 Pages 15701—15716
DOI https://doi.org/10.2147/JIR.S557031
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Ning Quan
Jingkai Tang,1,* Yiwei Zhang,1,* Yibing Wang,1,* Yanxin Fu,1 Jingman Qi,1 Aomeng Xiang,1 Ruoxuan Zhao,1 Ge Tan,1 Huili Deng,2 Xuchang Zhou,2 Liang Wu3
1Department of Sport Rehabilitation, Tianjin University of Sport, Tianjin, People’s Republic of China; 2Department of Rehabilitation Medicine, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, People’s Republic of China; 3Rehabilitation Medicine Department, Shougang Hospital Affiliated to Peking University, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Liang Wu, Email 1972wuliang@sina.com
Abstract: Alzheimer’s disease (AD) represents a progressive neurodegenerative disorder clinically defined by insidious multidomain cognitive deterioration and neuropathologically characterized by extracellular amyloid-β plaques and intraneuronal neurofibrillary tangles. Its pathological core includes β-amyloid protein (Aβ) deposition, neurofibrillary tangles (NFT) and neuroinflammation, seriously threatening the health of the elderly population worldwide. With the intensification of population aging, the socio-economic burden brought by AD is increasingly heavy. However, its complex pathogenesis has not been fully clarified, and there is an urgent need to explore new molecular markers and therapeutic targets. Lactylation, a novel metabolite-derived post-translational modification (PTM) where lactate groups are covalently conjugated to lysine residues, has recently been implicated in the pathological process of AD. For example, lactylation at histone H4 lysine 12 (H4K12la) has been reported to promote neuroinflammation via a “glycolysis/H4K12la/PKM2” positive feedback loop and activate the NLRP3 inflammasome-mediated pyroptosis. Similarly, lactylation at histone H3 lysine 18 (H3K18la) may enhance microglial activation through the NF-κB pathway. However, the role of lactylation in AD appears to be complex and context-dependent, as evidenced by seemingly contradictory findings regarding its impact on Aβ pathology. Therefore, this article reviews the relevant literature on lactylation and AD, summarizes the possible mechanisms by which lactylation regulates AD, and provides theoretical basis and reference for the related research on molecular markers and therapeutic targets of AD.
Keywords: lactylation, Alzheimer’s disease, post-translational modification
1Department of Sport Rehabilitation, Tianjin University of Sport, Tianjin, People’s Republic of China; 2Department of Rehabilitation Medicine, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, People’s Republic of China; 3Rehabilitation Medicine Department, Shougang Hospital Affiliated to Peking University, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Liang Wu, Email 1972wuliang@sina.com
Abstract: Alzheimer’s disease (AD) represents a progressive neurodegenerative disorder clinically defined by insidious multidomain cognitive deterioration and neuropathologically characterized by extracellular amyloid-β plaques and intraneuronal neurofibrillary tangles. Its pathological core includes β-amyloid protein (Aβ) deposition, neurofibrillary tangles (NFT) and neuroinflammation, seriously threatening the health of the elderly population worldwide. With the intensification of population aging, the socio-economic burden brought by AD is increasingly heavy. However, its complex pathogenesis has not been fully clarified, and there is an urgent need to explore new molecular markers and therapeutic targets. Lactylation, a novel metabolite-derived post-translational modification (PTM) where lactate groups are covalently conjugated to lysine residues, has recently been implicated in the pathological process of AD. For example, lactylation at histone H4 lysine 12 (H4K12la) has been reported to promote neuroinflammation via a “glycolysis/H4K12la/PKM2” positive feedback loop and activate the NLRP3 inflammasome-mediated pyroptosis. Similarly, lactylation at histone H3 lysine 18 (H3K18la) may enhance microglial activation through the NF-κB pathway. However, the role of lactylation in AD appears to be complex and context-dependent, as evidenced by seemingly contradictory findings regarding its impact on Aβ pathology. Therefore, this article reviews the relevant literature on lactylation and AD, summarizes the possible mechanisms by which lactylation regulates AD, and provides theoretical basis and reference for the related research on molecular markers and therapeutic targets of AD.
Keywords: lactylation, Alzheimer’s disease, post-translational modification