时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
Given the structural similarities between benzoate and SA, the hydrolysis product of ASA, we hypothesized that SA may modify the cellular proteins through Ksa (Fig. 1D), potentially contributing to the regulation of glucose metabolism and cell proliferation.Figure 1ASA treatment leads to cellular lysine salicylation.；Immunofluorescence staining showed that Ksa occurred predominantly in the nucleus and cytoplasm (Fig. 1H).To assess whether ASA elevates Ksa levels in vivo, we administered different doses of ASA to mice.；Given that the metabolite changes reversed at the F16BP-to-GAP step (Fig. 4A and B), we explored whether Ksa of ALDOA could influence its function, while acknowledging that ASA-induced acetylation and Ksa of other glycolytic enzymes might also contribute.
方法
Furthermore, a 3-year randomized trial revealed that low-dose ASA reduces the risk of recurrence in CRC patients harboring PI3K pathway mutations15.；In addition, cost-effectiveness studies support the use of ultra-low-dose ASA for secondary prevention in patients with a history of colorectal adenomas17.ASA consists of both acetyl and salicylate (SA) moieties and exerts its biological functions though two well-established mechanisms: covalent modification including N-acetylation and O-acetylation, and non-covalent inhibition of targets.；Although these studies have expanded our understanding of ASA's role in glycolysis, the underlying mechanisms remain incompletely understood.In this study, we show that ASA induces lysine salicylation (Ksa) at Lys13 of ALDOA, a glycolytic enzyme that converts F16BP to GAP.
核心结论
Beyond these, accumulating evidence indicates that ASA also exerts protective effects against cancer, particularly CRC9, 10, 11, 12.；A meta-analysis demonstrated that regular ASA use reduces CRC incidence in individuals over 70, especially those who began use before turning 7013.；Although these studies have expanded our understanding of ASA's role in glycolysis, the underlying mechanisms remain incompletely understood.In this study, we show that ASA induces lysine salicylation (Ksa) at Lys13 of ALDOA, a glycolytic enzyme that converts F16BP to GAP.
局限
However, current mechanisms cannot fully explain these results.；However, the mechanism of ASA-triggered salicylation remains unclear.；However, we cannot exclude the possibility of chemical acylation, particularly in basic environments such as those found in the mitochondria48, 49, 50.ASA shows inhibitory effects on glucose uptake and metabolism through multiple mechanisms33, including downregulating GLUT1 via NF-κB or NF-κB/HIF1α signaling51, acetylating glycolytic enzymes to inhibit their activity52,22, or reducing enzyme levels51,53.
对本项目的价值
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全文来源
PubMed PMC JATS（正文 49,770 字符，题名指纹 1.0，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：阿司匹林经 ALDOA 赖氨酸水杨酰化诱导糖酵解重编程
- 英文标题：Aspirin induces glycolytic reprogramming via lysine salicylation of ALDOA.
- 期刊与标识：Acta pharmaceutica Sinica. B · PMID 42979438 · DOI 10.1016/j.apsb.2026.07.002 · PMC PMC13729543