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Research Article | | Peer-Reviewed

Metabolic Function of Lactate and the Regulation and Biological Functions of Lactylation Modification

Linyue Hou,  Baosheng Sun,  Jinhui Sun,  Xueqin He,  Weixi Deng,  Yuneng Yang*
Published in Science Research (Volume 14, Issue 3)
Received: 16 April 2026     Accepted: 21 May 2026     Published: 29 May 2026
Views:       Downloads:
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Abstract

Lactate has long been regarded as a metabolic end product of glycolysis. However, recent studies have revealed its multiple functions in energy supply, signal transduction, and epigenetic regulation. This article systematically reviews the production, transport, and metabolic mechanisms of lactate, with an emphasis on its biological roles in immune regulation, inflammation control, intestinal homeostasis maintenance, and tumor microenvironment remodeling. In addition, it provides an in-depth discussion of the "writers-erasers-readers" regulatory network of lactylation. Lactylation is a lactate-driven post-translational modification that occurs on both histone and non-histone proteins. Histone lactylation primarily regulates gene transcription by altering chromatin conformation and plays key roles in macrophage polarization, inflammation resolution, and tumor progression. Non-histone lactylation extensively modifies various proteins, including metabolic enzymes and transcription factors, and participates in signal transduction, immune escape, and DNA repair. The two types of lactylation exhibit significant differences in modification sites, reaction mechanisms, and functional effects, together forming an important bridge between metabolism and epigenetic regulation. Current studies suggest that targeting lactate metabolism or lactylation-related regulatory pathways holds therapeutic potential in tumors, inflammatory diseases, and metabolic disorders. Future efforts are needed to further elucidate the dynamic regulatory networks of lactylation under pathological conditions and to facilitate its clinical translation.

Published in Science Research (Volume 14, Issue 3)
DOI 10.11648/j.sr.20261403.11
Page(s) 62-70
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2026. Published by Science Publishing Group
Previous article
Keywords

Lactate, Lactylation, Histone, Non-histone

1．引言
乳酸长期以来被视为糖酵解的代谢终产物。然而，近年来的研究逐渐揭示了乳酸在能量代谢、信号转导和表观遗传调控中的多重功能。特别是2019年Zhang等首次发现乳酸可驱动组蛋白赖氨酸残基发生乳酰化修饰，这一突破性发现为理解代谢重塑与基因表达调控之间的联系提供了全新视角
[1]
。随后，研究者相继鉴定了p300等乳酰化“writers（书写器）”、HDAC1-3等“erasers（擦除器）”以及Brg1等“readers（读取器）”，初步勾勒出乳酰化修饰的酶调控网络
[2-4]
。此外，乳酰化不仅局限于组蛋白，也广泛修饰非组蛋白，参与肿瘤代谢重编程、免疫逃逸及炎症调控等关键生物学过程
[5]
。尽管乳酰化修饰的研究取得了快速进展，但目前对其调控机制的认知仍处于起步阶段。不同乳酰化“书写器”、“擦除器”与“读取器”的底物特异性、乳酰化修饰在不同生理病理条件下的动态变化规律，以及组蛋白乳酰化与非组蛋白乳酰化在功能上的协同与差异，均有待深入探讨。
基于此，本文系统综述了乳酸的生成、转运与代谢功能，重点阐述了乳酰化修饰的writers-erasers-readers调控网络及其在组蛋白与非组蛋白中的机制差异，总结了乳酰化在基因表达调控、免疫调节、DNA修复及肿瘤进展中的关键作用，并对靶向该通路的治疗潜力进行展望，以期为相关领域的深入研究提供理论参考。
2．乳酸的生成、转运与代谢
2.1．乳酸的生成
乳酸主要通过糖酵解、谷氨酰胺代谢两种途径生成
[6]
。(1)糖酵解途径：缺氧条件下，葡萄糖经氧化生成丙酮酸，随后由乳酸脱氢酶催化还原为乳酸
[7, 8]
。注意的是，即便在有氧条件下，部分高增殖细胞（如肿瘤细胞）仍偏好糖酵解而非氧化磷酸化途径获取能量，导致乳酸积累，这一现象被称为有氧糖酵解或瓦博格效应（Warburg effect）
[9, 10]
。(2)谷氨酰胺进入线粒体参与三羧酸循环，也生成乳酸
[6]
。
Figure 1. 图1 肠道中的乳酸代谢（图片引自文献
[18]
）。
此外，乳杆菌和双歧杆菌等产乳酸菌
[11, 12]
，能够通过碳水化合物发酵产生乳酸
[13]
。而乳酸利用菌则利用乳酸生成短链脂肪酸包括乙酸、丙酸和丁酸
[14, 15]
。例如，厌氧丁酸菌属（Anaerobutyricum）能够将乳酸转化为丙酸或丁酸
[16]
，丙酸主要由韦荣球菌属（Veillonella）通过琥珀酸途径生成
[17, 18]
（图1）。
2.2．乳酸转运与代谢
乳酸穿梭是指乳酸在细胞、组织和器官之间的转运过程
[6]
；主要由单羧酸转运蛋白（MCTs）
[19]
和钠偶联单羧酸转运蛋白（SMCTs）
[2, 20]
介导。其中，MCT4主要在高糖酵解活性的细胞（如癌细胞）中表达
[6]
，负责将乳酸外排至胞外环境
[7]
。而MCT1
[21]
和SMCTs（包括SMCT1和SMCT2）
[2, 20]
则在心肌、脑等高耗能组织中负责摄取乳酸。进入细胞后，乳酸主要通过以下两条途径代谢
[22]
：(1)在乳酸脱氢酶的催化下氧化为丙酮酸，随后进入线粒体参与三羧酸循环，最终彻底氧化并生成ATP；(2)在肝脏等组织中经糖异生途径重新转化为葡萄糖。
3．乳酸的功能
乳酸具备广泛的生物学功能，能调节能量代谢、抑制致病菌增殖以及作为信号转导分子参与免疫反应及细胞间通讯等过程。
3.1．供能作用
乳酸作为可循环的能量载体和葡萄糖再生的前体，通过乳酸穿梭为全身全身各组织（尤其大脑）提供能量。最新研究发现，乳酸可以不依赖于代谢途径直接进入线粒体，激活电子传递链，从而促进ATP的合成
[23]
。
3.2．抑菌作用
乳酸可通过降低胃肠道的pH，抑制不耐酸的致病菌的增殖
[24]
。此外，它还能增加革兰氏阴性菌的细胞膜通透性，从而发挥抗菌作用
[25, 26]
。同时，乳酸可通过调节肠道菌群结构，维持肠道微生态稳定，增强对病原微生物的抵御能力
[27]
。
3.3．信号转导功能
乳酸作为关键的信号分子，广泛参与细胞信号传导过程
[22, 28]
。它可作为配体与细胞膜上的G蛋白偶联受体包括GPR81
[12, 22, 29]
和GPR132
[20]
，进而启动下游信号级联反应。乳酸通过GPR81和GPR132
[6]
、GPR31
[2]
等受体调控免疫细胞功能，抑制免疫反应并促进免疫逃逸。研究发现，乳酸激活GPR81后可下调cAMP-PKA信号通路，介导免疫抑制效应
[7]
；也可通过mTOR/HIF-1α/STAT3轴激活髓源性抑制细胞，增强免疫抑制并削弱抗肿瘤免疫
[30]
。此外，乳酸通过激活GPR132促进M2型巨噬细胞分化，推动肿瘤的进展与转移
[8]
。
除免疫调节外，乳酸信号也在其他生理过程中发挥作用。例如，脂肪组织中的GPR81感应乳酸后可抑制脂肪分解并促进脂肪生成
[8]
；内皮细胞GPR81感应乳酸，则会降低血管内皮-钙粘蛋白的表达，增强骨髓血管通透性
[20]
。
3.4．调节炎症作用
乳酸参与调节多种与炎症进展相关的细胞信号通路
[22]
。研究表明，乳酸可抑制Toll样受体（TLR）介导的单核巨噬细胞活化，延缓蛋白激酶B（Akt）的去磷酸化过程，抑制促炎细胞因子包括肿瘤坏死因子α (TNF-α)、白细胞介素23（IL-23）和趋化因子配体2（CCL2）和CCL7的分泌，从而抑制炎症反应、维持宿主健康
[31]
。然而，也有研究表明，乳酸在Toll样受体刺激下促进单核细胞和巨噬细胞中IL-23的转录，进而维持IL-23依赖的IL-17分泌
[29]
。
3.5．对免疫细胞的调节作用
乳酸可影响巨噬细胞、树突状细胞和T细胞等多种免疫细胞的活性，参与营造免疫抑制微环境
[7]
。研究表明，乳酸通过激活ERK/STAT3通路，促进促炎性的M1型巨噬细胞向抗炎性的M2型极化
[7, 32]
。此外，乳酸还可诱导肌肉组织中的M2巨噬细胞活化，从而促进组织修复与生长
[33, 34]
。
3.6．对肿瘤的双重调控作用
乳酸在肿瘤进展中扮演着双重角色。一方面，乳酸可促进肿瘤的生长、转移和治疗抵抗
[6]
。作为肿瘤细胞的关键能量底物，乳酸通过“乳酸穿梭”在肿瘤中积累，形成有利于肿瘤生长的酸性环境
[1, 6]
。同时，乳酸还可以通过抑制免疫细胞并增强调节性T细胞等免疫抑制细胞的功能，削弱机体的抗肿瘤免疫应答
[7, 35]
。另一方面，乳酸亦可通过调节免疫细胞的代谢状态，增强抗肿瘤活性，显示出它在肿瘤免疫调控中的复杂性与多面性
[6]
。
3.7．促肠道干细胞再生
研究发现，乳酸通过激活潘氏细胞和基质细胞表面的受体GPR81，并协同Wnt3/β-catenin通路，调节Lgr5+肠干细胞的增殖和分化，从而促进上皮细胞再生
[36]
。相似研究表明，Lgr5+肠干细胞可将潘氏细胞产生的乳酸转化为丙酮酸，随后通过线粒体氧化磷酸化产生活性氧，激活p38信号通路，调控干细胞的更新分化
[37, 38]
。
4．乳酰化
4.1．定义
乳酰化（Lactylation）是指乳酸与蛋白质赖氨酸残基上的ε-氨基共价结合，形成乳酰化赖氨酸的修饰过程
[22, 28]
，亦称为赖氨酸乳酰化(Lysine Lactylation，Kla)。它是一种新型的表观遗传修饰，属于翻译后修饰（post-translational modification，PTM），已逐渐成为代谢与表观遗传交叉领域的研究前沿
[39]
。
4.2．乳酰化的调控机制
乳酰化修饰过程受到“书写器”（writers）、“擦除器”（erasers）和“读取器”（readers）三类调控因子的协同作用（图2）
[5, 7]
，这对于维持细胞的能量代谢和信号传递的准确性至关重要。
Figure 2. 图2 乳酸介导赖氨酸乳酰化的分子通路示意图（图片引自文献
[7]
）。
图释：在胞内微环境中，乳酸通过酶催化途径转化为乳酰辅酶A，或经由非酶促化学机制，作为底物参与蛋白质赖氨酸残基的乳酰化修饰。该翻译后修饰过程由组蛋白乙酰转移酶p300催化完成（书写器功能），而组蛋白去乙酰化酶家族成员则执行去乳酰化修饰（擦除器功能）。特异性阅读蛋白可识别组蛋白乳酰化表观遗传标记，进而通过染色质重塑机制调控下游基因转录程序与免疫信号网络（读取器功能）。缩写注释：LDH 乳酸脱氢酶；TCA 三羧酸循环；Kla 赖氨酸乳酰化；HDACs 组蛋白去乙酰化酶；P300 E1A结合蛋白p300；La 乳酸；Reader 读取器。
（1）writers（书写器），是指催化乳酰化修饰反应的酶或蛋白质
[2]
，主要包括经典的组蛋白乙酰转移酶（如p300、CBP、KAT8、HBO1、Tip60和KAT2）
[22]
，以及丙氨酰-tRNA合成酶（AARS1和AARS2）
[5]
。p300等组蛋白乙酰转移酶兼具乳酸酰基转移酶活性，它们可利用乳酰辅酶A（lactyl-CoA）作为底物，将乳酰基转移至赖氨酸残基的ε-氨基上进行乳酰化修饰（酶促途径）
[2, 5]
；也通过乳酰谷胱甘肽转移乳酰基团进行修饰（非酶促途径）
[8, 21]
。
与p300等乙酰转移酶不同，丙氨酰-tRNA合成酶AARS1和AARS2具有乳酸感知蛋白的功能并表现出乳酸转移酶的活性
[2, 40]
，二者并不依赖乳酰辅酶A作为底物，而是直接结合乳酸，并以ATP依赖的方式形成乳酸-AMP中间体，进而将乳酰基团转移至靶蛋白赖氨酸残基，介导蛋白质赖氨酸乳酰化修饰
[4, 40]
。
此外，乳酰辅酶A合成酶ACSS2和GTPSCS能将乳酸转化为乳酰辅酶A，为“writers”提供关键底物，在启动乳酰化修饰过程中发挥重要作用
[2, 5]
。
（2）erasers（擦除器），是指能够去除乳酰化修饰基团的酶或蛋白质
[21]
，主要包括I类组蛋白去乙酰化酶（HDAC1、HDAC2和HDAC3）和III类蛋白去乙酰化酶（SIRT1、SIRT2、SIRT3）
[1, 2, 5]
。HDAC1-3是体外最有效的“eraser”，其中HDAC3活性最强
[41]
；它们具有位点特异性去乳酰化活性，能够有效降低H3K18和H4K5位点的乳酰化水平
[42]
。
（3）readers（读取器），是指能特异性识别并结合乳酰化修饰位点的蛋白质，如Brg1、DPF2
[5]
和TRIM33
[2]
等。它们通过识别乳酰化修饰，调控下游信号通路，进而影响细胞的生理功能。例如，Brg1通过结合H3K18乳酰化位点调控MET基因转录
[42]
；DPF2则结合H3K14la，促进致癌基因的转录。
4.3．乳酰化的作用
4.3.1．调控基因表达
乳酰化可改变染色质可及性，影响基因转录与蛋白质功能
[2, 43, 44]
。此外，乳酰化还与乙酰化等表观遗传学修饰相互作用，协同调控基因表达
[45]
。
4.3.2．参与DNA损伤修复
研究表明，乳酰化能够直接调控同源重组过程，进而精确修复DNA双链断裂这一严重损伤形式
[2]
。
4.3.3．调节代谢途径
乳酰化可抑制线粒体酶的活性，阻断柠檬酸循环，从而限制氧化磷酸化及活性氧的生成
[2]
。除了糖酵解外，乳酰化还参与磷酸戊糖途径、脂肪酸代谢和氨基酸代谢等过程。
4.3.4．参与信号传导
乳酰化在多种信号通路的调控中具有重要作用，可影响细胞增殖、自噬与免疫应答等过程
[46]
。研究显示，乳酸可通过诱导细胞外信号调节激酶（ERK）发生乳酰化修饰，进一步激活丝裂原活化蛋白激酶（MAPK）通路，从而促进肿瘤进展
[3]
。
4.3.5．调节免疫反应
研究表明，糖酵解产生的乳酸可升高组蛋白H3第18位赖氨酸乳酰化（H3K18la）水平，从而激活组织修复相关基因的表达
[2]
。此外，在炎症后期，乳酰化可促进巨噬细胞由M1型向M2型转化，参与炎症消退和组织修复过程
[7]
。而在脓毒症等全身性炎症反应中，乳酸介导的乳酰化水平升高则可能加剧病情发展
[2]
。
4.3.6．在肿瘤中的作用
乳酰化可激活免疫细胞中的抑制性通路，重塑肿瘤微环境，并通过调控肿瘤代谢重编程与免疫逃逸机制，促进肿瘤生长
[1]
。例如，乳酸可经AARS1催化肿瘤抑制因子p53发生位点特异性乳酰化修饰，降低其DNA结合能力，从而促进肿瘤的发生发展
[46]
。然而，研究也表明乳酰化可调控转化生长因子-β和细胞凋亡等信号通路，在一定条件下发挥抗肿瘤作用
[8]
。
4.4．组蛋白乳酰化
4.4.1．定义
乳酰化包括组蛋白乳酰化和非组蛋白乳酰化。乳酸可共价修饰组蛋白赖氨酸残基，这一过程称为组蛋白乳酰化（histone lactylation）
[1, 21]
。
4.4.2．调控酶
组蛋白乳酰化依赖于调控酶writer、eraser和reader的调控（图3）。此外，细胞内乳酸水平也会以剂量依赖性方式影响该修饰：糖酵解抑制剂可通过降低乳酸含量抑制组蛋白乳酰化，而补充葡萄糖或使用线粒体抑制剂则通过提高乳酸水平促进乳酰化
[42]
。
Figure 3. 图3影响组蛋白乳酰化水平的代谢物与修饰酶（图片引自文献
[42]
）。
图释：在糖酵解过程中产生或通过MCT1转运蛋白运输的乳酸，显著影响组蛋白乳酰化水平。糖酵解抑制剂通过降低乳酸水平减少乳酰化，而线粒体抑制剂则通过提升乳酸浓度增强乳酰化。组蛋白乳酰化水平受Brg1等识别蛋白调控，并被HDAC1、HDAC3等擦除酶调节。此外，p300催化组蛋白乳酰化；其表达水平的改变可相应提高或降低组蛋白乳酰化水平。
4.4.3．组蛋白乳酰化的功能
组蛋白乳酰化参与调控基因表达、DNA修复
[29]
、信号通路及肿瘤生长等多个生物学过程。
（1）调控基因表达
组蛋白是细胞核内负责DNA包装与染色质组成的基本蛋白质
[21]
。组蛋白乳酰化可通过改变组蛋白结构，影响染色质构象及DNA可及性，进而调控基因表达
[1, 47, 48]
。当组蛋白H3或H4的赖氨酸残基被突变为精氨酸时，改效应消失，进一步突显了组蛋白乳酰化在基因激活中的关键作用
[2]
。
在已知的组蛋白乳酰化位点中，H3K18la的作用最为明确。例如，在巨噬细胞向M2型极化过程中，H3K18la可激活精氨酸酶1（Arg1）、kruppel样因子4（Klf4）等基因的转录，从而增强巨噬细胞的抗炎与组织修复功能
[1, 49, 50]
。
（2）调节免疫反应
组蛋白乳酰化调控免疫细胞功能，进而重塑全身性炎症反应
[7]
。研究表明，乳酸生成与组蛋白乳酰化在训练免疫的诱导与维持过程中具有核心作用
[51]
。
（3）调控巨噬细胞表型转换
组蛋白乳酰化是巨噬细胞从M1型向M2型转换的关键“分子开关”
[29]
。
乳酸通过诱导巨噬细胞组蛋白乳酰化，进而调控相关基因表达，推动巨噬细胞由促炎、抗肿瘤的M1型转变为抗炎、促肿瘤的M2型表型
[1]
。研究者发现，M1型巨噬细胞内存在“乳酸时钟”调控机制
[1, 21]
：其细胞内的乳酸通过三羧酸循环转化为乳酰辅酶A，后者进入细胞核启动“乳酸时钟”
[21]
，激活ARG1等M2型特征基因的表达
[1, 21]
，促使巨噬细胞获得M2型属性
[6]
。此外，M1巨噬细胞中的乳酸积累也可诱导丙酮酸激酶M2发生乳酰化，激活其四聚体形式，抑制糖酵解通量，进一步推动M2型表型转换
[6]
。
Figure 4. 图4 乳酰化促进肿瘤发生的机制（图片引自文献
[22]
）。
图释：乳酰化通过维持TAM（肿瘤相关巨噬细胞）稳态导致肿瘤免疫抑制；直接促进肿瘤细胞内致癌基因YTHDF2的表达；维持肿瘤细胞代谢稳态；并可能通过抑制肿瘤微环境（TME）中多种免疫细胞功能，导致肿瘤免疫抑制与免疫逃逸。缩写：HK-1，己糖激酶-1；G6PD，葡萄糖-6-磷酸脱氢酶；PKM，丙酮酸激酶；SDH，琥珀酸脱氢酶；IDH，异柠檬酸脱氢酶。
（4）在肿瘤中的作用
组蛋白乳酰化参与肿瘤代谢重编程与免疫逃逸过程
[9]
。研究表明，组蛋白乳酰化可调控肿瘤相关基因（如致癌基因YTHDF2）的转录，促进下游肿瘤抑制因子的降解，从而驱动肿瘤的生长、转移与侵袭
[22]
（图4）。例如，组蛋白的修饰位点H3K18la可激活MYC等癌基因
[52]
或抑制某些抑癌基因的表达，进而促进肿瘤细胞增殖
[53]
。此外，乳酸还可通过诱导组蛋白乙酰化，激活BRD4-MYC信号轴，进一步增强肿瘤细胞的表型可塑性
[52]
。
4.5．非组蛋白乳酰化
除组蛋白外，乳酸还可诱导代谢酶、转录因子等多种非组蛋白发生乳酰化修饰，即非组蛋白乳酰化
[7]
。该修饰可通过改变蛋白质的构象、稳定性及其分子间相互作用，进而在基因表达调控、细胞信号转导和代谢稳态等关键生物学过程中发挥重要作用。非组蛋白乳酰化的发现，表明乳酸的信号调控功能已从染色质层面扩展至近乎所有细胞生命活动领域
[6]
。
4.5.1．组蛋白与非组蛋白乳酰化的区别
Figure 5. 图5两种不同的乳酰化生成方式（图片引自文献
[21]
）。
图释：Kla（乳酰化修饰）包括KL-la和KD-la两种经典形式。L-乳酸可进入细胞核介导组蛋白乳酰化，还能通过酶促反应修饰非组蛋白。D-乳酸则经非酶促过程修饰非组蛋白。
组蛋白乳酰化（前者）与非组蛋白乳酰化（后者），在修饰靶点、反应类型及功能机制等方面存在明显的区别
[5]
。（1）修饰位点：前者主要发生在H2A、H2B、H3和H4等核心组蛋白上，已鉴定出28个修饰位点，其中以H3K18la和H4K12la研究最为深入；后者则广泛分布于酶和转录因子等，已发现9000多个修饰位点，如AARS1-K120la。（2）反应类型与功能机制：前者主要依赖L-乳酸驱动的酶促反应，通过改变染色质构象调控基因转录；后者则通过L-乳酸/D-乳酸的酶促或非酶促途径启动，主要通过调节蛋白质的活性、稳定性或相互作用来发挥功能
[5]
（图5）。（3）生物学意义：前者聚焦表观遗传调控，后者则广泛涉及代谢调控、信号传导、DNA修复等多样化细胞过程。
4.5.2．非组蛋白乳酰化的生物学功能
非组蛋白乳酰化在免疫逃逸、代谢重编程以及炎症与修复平衡过程中发挥重要调控作用。研究发现，AARS2可对环鸟苷酸-腺苷酸合成酶（cGAS）进行非组蛋白乳酰化修饰，抑制其活性
[40]
，减少了干扰素的产生，促进了病毒的免疫逃逸
[54]
。
非组蛋白乳酰化促进高迁移率族蛋白B1（HMGB1）从细胞核向细胞质转位
[7]
，HMGB1随后以外泌体形式分泌，诱导内皮功能障碍并加重脓毒症进展
[55]
。这表明，非组蛋白乳酰化可不依赖染色质重塑，直接调控免疫与炎症反应。此外，非组蛋白乳酰化还可通过修饰Yes相关蛋白1（YAP）等多种底物蛋白，参与促进细胞增殖、增强DNA修复能力以及诱导化疗耐药等过程
[8]
。
5. 总结与展望
乳酸及其衍生的乳酰化修饰构成了细胞代谢与表观遗传调控的关键桥梁。乳酸不仅是能量底物和信号分子，还通过乳酰化直接调控染色质与蛋白质功能，影响基因表达、DNA修复及代谢重编程等过程。组蛋白乳酰化主要调控转录，而非组蛋白乳酰化则广泛参与信号传导、免疫应答与代谢稳态，共同拓展了乳酸的调控维度。未来需进一步揭示病理条件下乳酰化的动态调控网络，并探索靶向该通路在肿瘤、炎症及代谢性疾病中的治疗前景，推动其临床转化。
致谢
本论文获2024年贵州省职业教育“技能贵州”行动计划项目“省级畜牧兽医专业群教师教学创新团队”（黔教函〔2024〕44号）、遵义市微生物发酵饲料科技创新团队建设项目（遵KCTD〔2024〕055号）和“技能贵州—现代农业市域产教联合体”的资助。
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    Hou, L., Sun, B., Sun, J., He, X., Deng, W., et al. (2026). Metabolic Function of Lactate and the Regulation and Biological Functions of Lactylation Modification. Science Research, 14(3), 62-70. https://doi.org/10.11648/j.sr.20261403.11

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    Hou, L.; Sun, B.; Sun, J.; He, X.; Deng, W., et al. Metabolic Function of Lactate and the Regulation and Biological Functions of Lactylation Modification. Sci. Res. 2026, 14(3), 62-70. doi: 10.11648/j.sr.20261403.11

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    Hou L, Sun B, Sun J, He X, Deng W, et al. Metabolic Function of Lactate and the Regulation and Biological Functions of Lactylation Modification. Sci Res. 2026;14(3):62-70. doi: 10.11648/j.sr.20261403.11

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  • @article{10.11648/j.sr.20261403.11,
  author = {Linyue Hou and Baosheng Sun and Jinhui Sun and Xueqin He and Weixi Deng and Yuneng Yang},
  title = {Metabolic Function of Lactate and the Regulation and Biological Functions of Lactylation Modification},
  journal = {Science Research},
  volume = {14},
  number = {3},
  pages = {62-70},
  doi = {10.11648/j.sr.20261403.11},
  url = {https://doi.org/10.11648/j.sr.20261403.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sr.20261403.11},
  abstract = {Lactate has long been regarded as a metabolic end product of glycolysis. However, recent studies have revealed its multiple functions in energy supply, signal transduction, and epigenetic regulation. This article systematically reviews the production, transport, and metabolic mechanisms of lactate, with an emphasis on its biological roles in immune regulation, inflammation control, intestinal homeostasis maintenance, and tumor microenvironment remodeling. In addition, it provides an in-depth discussion of the "writers-erasers-readers" regulatory network of lactylation. Lactylation is a lactate-driven post-translational modification that occurs on both histone and non-histone proteins. Histone lactylation primarily regulates gene transcription by altering chromatin conformation and plays key roles in macrophage polarization, inflammation resolution, and tumor progression. Non-histone lactylation extensively modifies various proteins, including metabolic enzymes and transcription factors, and participates in signal transduction, immune escape, and DNA repair. The two types of lactylation exhibit significant differences in modification sites, reaction mechanisms, and functional effects, together forming an important bridge between metabolism and epigenetic regulation. Current studies suggest that targeting lactate metabolism or lactylation-related regulatory pathways holds therapeutic potential in tumors, inflammatory diseases, and metabolic disorders. Future efforts are needed to further elucidate the dynamic regulatory networks of lactylation under pathological conditions and to facilitate its clinical translation.},
 year = {2026}
}

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  • TY  - JOUR
T1  - Metabolic Function of Lactate and the Regulation and Biological Functions of Lactylation Modification
AU  - Linyue Hou
AU  - Baosheng Sun
AU  - Jinhui Sun
AU  - Xueqin He
AU  - Weixi Deng
AU  - Yuneng Yang
Y1  - 2026/05/29
PY  - 2026
N1  - https://doi.org/10.11648/j.sr.20261403.11
DO  - 10.11648/j.sr.20261403.11
T2  - Science Research
JF  - Science Research
JO  - Science Research
SP  - 62
EP  - 70
PB  - Science Publishing Group
SN  - 2329-0927
UR  - https://doi.org/10.11648/j.sr.20261403.11
AB  - Lactate has long been regarded as a metabolic end product of glycolysis. However, recent studies have revealed its multiple functions in energy supply, signal transduction, and epigenetic regulation. This article systematically reviews the production, transport, and metabolic mechanisms of lactate, with an emphasis on its biological roles in immune regulation, inflammation control, intestinal homeostasis maintenance, and tumor microenvironment remodeling. In addition, it provides an in-depth discussion of the "writers-erasers-readers" regulatory network of lactylation. Lactylation is a lactate-driven post-translational modification that occurs on both histone and non-histone proteins. Histone lactylation primarily regulates gene transcription by altering chromatin conformation and plays key roles in macrophage polarization, inflammation resolution, and tumor progression. Non-histone lactylation extensively modifies various proteins, including metabolic enzymes and transcription factors, and participates in signal transduction, immune escape, and DNA repair. The two types of lactylation exhibit significant differences in modification sites, reaction mechanisms, and functional effects, together forming an important bridge between metabolism and epigenetic regulation. Current studies suggest that targeting lactate metabolism or lactylation-related regulatory pathways holds therapeutic potential in tumors, inflammatory diseases, and metabolic disorders. Future efforts are needed to further elucidate the dynamic regulatory networks of lactylation under pathological conditions and to facilitate its clinical translation.
VL  - 14
IS  - 3
ER  -

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