时间标签：数据日期 2026-11-01 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31–2026/11/01 ｜ 情报发生日期 2026-11-01
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
研究问题
The brain, as a highly metabolically active organ, depends on mitochondrial oxidative phosphorylation (OXPHOS) to sustain energy demands.
方法
When mitochondrial function is impaired, cells undergo metabolic reprogramming toward aerobic glycolysis, leading to lactate accumulation.
核心结论
Beyond its traditional role as a metabolic byproduct, lactate is now recognized as a signaling molecule that links metabolism to epigenetic regulation through protein lactylation, a post-translational modification identified by Zhang et al. in 2019.；Research on lactylation has progressed through three stages: initial discovery in histone lactylation as an epigenetic mark, expansion to non-histone proteins revealing roles in metabolic and structural regulation, and recent identification of mitochondrial…；This review summarizes the mitochondrial-lactate-lactylation axis in the nervous system, including brain lactate metabolism, the astrocyte-neuron lactate shuttle, and regulatory mechanisms of lactylation (writers, erasers, and readers).
局限
（原文未给出可直接抽取的对应表述）
对本项目的价值
临床前机制证据，需评估物种外推与剂量可行性：线粒体是衰老干预的共同下游效应器，可用于跨器官效应的统一读数。 ｜ 价值分 1.9/5（★★☆☆☆）
全文来源
未取到全文 → 本卡为摘要级解读，未核验全文
原文题录
- 英文标题：Mitochondrial Lactate Signaling and Protein Lactylation in Neurological Diseases.
- 期刊与标识：Molecular neurobiology · PMID 42955568 · DOI 10.1007/s12035-026-06291-z
C 级证据分级：C 级（预印本 / 观点评论，非原始研究）
本文属观点/评论类文献，不是原始研究。其论点依赖于作者对既有证据的梳理与判断，不构成新的实验证据。本站标注 C 级即为此意——阅读时请把它当作「领域内的思考框架」，而非「研究发现」。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」（SOP §4.2 摘要级）撰写，依据期刊公开摘要与 PubMed 元数据；付费墙全文未获取之处已标注「待补全文」，未做任何数值推算补全。