超级增强子与肥胖相关代谢性疾病的研究进展

doi:10.11852/zgetbjzz2025-0299

中国儿童保健杂志 ›› 2025, Vol. 33 ›› Issue (10): 1079-1081.DOI: 10.11852/zgetbjzz2025-0299

超级增强子与肥胖相关代谢性疾病的研究进展

王同帅, 郭锡熔

上海市同仁医院,上海交通大学医学院附属同仁医院,虹桥国际医学研究院,上海 200336

收稿日期:2025-03-27 修回日期:2025-06-16 发布日期:2025-10-11
通讯作者: 郭锡熔,E-mail:xrguo@shsmu.edu.cn
作者简介:王同帅(1990—),男,助理研究员,博士研究生,主要研究方向为环境污染物致机体代谢性效应改变评估及其调控机制。
基金资助:
国家重点研发计划(2021YFC2701900;2021YFC2701903);国家自然科学基金项目(82170869)

Super enhancers in obesity-related metabolic diseases

WANG Tongshuai, GUO Xirong

Hongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China

Received:2025-03-27 Revised:2025-06-16 Published:2025-10-11
Contact: GUO Xirong,E-mail:xrguo@shsmu.edu.cn

摘要/Abstract

摘要： 超级增强子(SE)是基因组中重要的大片段顺式调控元件,通过显著增强基因转录效率发挥基因调控作用。细胞内数百个SE协同调控大量关键基因,其异常活化与糖尿病、炎症和肿瘤等多种疾病的发生密切相关。然而,SE在代谢性疾病中的调控机制研究仍相对滞后。代谢性疾病不仅是多种慢性病的早期诱因,也是肿瘤发生的关键风险因素,被视为疾病发生的“共同土壤”。深入研究SE在代谢性疾病中的作用机制,可为完善疾病防治策略提供科学依据。本文就SE在代谢性疾病中的作用与机制进行综述,以期为开展相关基础研究和开拓临床应用提供依据。

关键词: 超级增强子, 肥胖, 转录调控, 调节元件, 代谢性疾病

Abstract: Super-enhancers (SEs) are specialized DNA elements that significantly enhance transcriptional efficiency, driving the expression of genes essential for cellular function.Each cell contains hundreds of SEs, which regulate key gene networks.Dysregulation of SEs has been implicated in the aberrant activation of pathogenic genes in diseases such as Alzheimer's, diabetes, inflammation, and cancer.Despite their significance, the role of SEs in metabolism-related diseases remains underexplored.Metabolic disorders often serve as foundational factors in the development of other chronic conditions.Understanding the involvement of SEs in the initiation and progression of metabolic diseases could provide critical insights and inform the development of effective prevention strategies.This review explores the emerging role of SEs in metabolic disorders and their potential as targets for therapeutic intervention.

Key words: super-enhancers, obesity, transcription, regulatory elements, metabolism

中图分类号:

R179

王同帅, 郭锡熔. 超级增强子与肥胖相关代谢性疾病的研究进展[J]. 中国儿童保健杂志, 2025, 33(10): 1079-1081.

WANG Tongshuai, GUO Xirong. Super enhancers in obesity-related metabolic diseases[J]. Chinese Journal of Child Health Care, 2025, 33(10): 1079-1081.

参考文献

[1] Hnisz D, Abraham BJ, Lee TI, et al.Super-enhancers in the control of cell identity and disease[J].Cell, 2013, 155(4): 934-947.
[2] Whyte WA, Orlando DA, Hnisz D, et al.Master transcription factors and mediator establish super-enhancers at key cell identity genes[J].Cell, 2013, 153(2): 307-319.
[3] Cao HB, Zhuo R, Zhang ZM, et al.Super-enhancer-associated INSM2 regulates lipid metabolism by modulating mTOR signaling pathway in neuroblastoma[J].Cell Biosci, 2022, 12(1): 1.
[4] Zhang F, Li Z, Fang F, et al.IRF1 is a core transcriptional regulatory circuitry member promoting AML progression by regulating lipid metabolism[J].Exp Hematol Oncol, 2025, 14(1): 25.
[5] Selivanovskiy AV, Molodova MN, Khrameeva EE, et al.Liquid condensates: A new barrier to loop extrusion?[J].Cell Mol Life Sci, 2025, 82(1): 80.
[6] Zhang S, Wang C, Qin S, et al.Analyzing super-enhancer temporal dynamics reveals potential critical enhancers and their gene regulatory networks underlying skeletal muscle development[J].Genome Res, 2024, 34(12): 2190-2202.
[7] Yang RY, Wu YY, Ming Y, et al.A super-enhancer maintains homeostatic expression of Regnase-1[J].Gene, 2018, 669: 35-41.
[8] Peng JY, Cai DK, Zeng RL, et al.Upregulation ofsuperenhancer-driven LncRNA FASRL by USF1 promotes de novo fatty acid biosynthesis to exacerbate hepatocellular carcinoma[J].Adv Sci, 2022, 10(1): e2204711.
[9] Lai B, Lee JE, Jang Y, et al.MLL3/MLL4 are required for CBP/p300 binding on enhancers and super-enhancer formation in brown adipogenesis[J].Nucleic Acids Res, 2017, 45(11): 6388-6403.
[10] Watanabe-Takano H, Ochi H, Chiba A, et al.Mechanical load regulates bone growth via periosteal osteocrin[J].Cell Rep, 2021, 36(2): 109380.
[11] Hnisz D, Abraham BJ, Lee TI, et al.Super-enhancers in the control of cell identity and disease[J].Cell, 2013, 155(4): 934-947.
[12] Kuo T, Kraakman MJ, Damle M, et al.Identification of as a human diabetes susceptibility gene with a role in β cell insulin secretion[J].Proc Natl Acad Sci USA, 2019, 116(40): 20033-20042.
[13] Chim SM, Howell K, Dronzek J, et al.Genetic inactivation of zinc transporter SLC39A5 improves liver function and hyperglycemia in obesogenic settings[J].Elife, 2024, 12: 1.
[14] Sengupta S, George RE.Super-enhancer-driven transcriptional dependencies in cancer[J].Trends Cancer, 2017, 3(4): 269-281.
[15] Zhang LY, Wang CY, Xu Q, et al.Removal of epigenetic repressive mark on inflammatory genes in fat liver[J].J Gastroenterol Hepatol, 2023, 38(8): 1426-1437.
[16] Liu M, Cao S, He L, et al.Super enhancer regulation of cytokine-induced chemokine production in alcoholic hepatitis[J].Nat Commun, 2021, 12(1): 4560.
[17] Bartolome A.Stem cell-derived beta cells: A versatile research platform to interrogate the genetic basis of beta cell dysfunction[J].Int J Mol Sci, 2022, 23(1): 1.
[18] Ma H, Qu J, Pang Z, et al.Super-enhancer omics in stem cell[J].Mol Cancer, 2024, 23(1): 153.
[19] Xu X, Brasier AR.SMARCA4 regulates inducible BRD4 genomic redistribution coupling intrinsic immunity and plasticity in epithelial injury-repair[J].Nucleic Acids Res, 2025, 53(6): 1.
[20] Wang C, Tian W, Hu SY, et al.Lineage-selective super enhancers mediate core regulatory circuitry during adipogenic and osteogenic differentiation of human mesenchymal stem cells[J].Cell Death Dis, 2022, 13(10): 866.
[21] Rothhammer V, Mascanfroni ID, Bunse L, et al.Type I interferons and microbial metabolites of tryptophan modulate astrocyte activity and central nervous system inflammation via the aryl hydrocarbon receptor[J].Nat Med, 2016, 22(6): 586-597.

超级增强子与肥胖相关代谢性疾病的研究进展

Super enhancers in obesity-related metabolic diseases

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 15

编辑推荐

Metrics

[1]	方春丽, 章志红, 刘梦娇. 支链氨基酸与母子间超重肥胖代际传递的关系[J]. 中国儿童保健杂志, 2025, 33(9): 992-996.
[2]	许玥, 郜统勋, 胡思源, 李梅芳, 栾奕博, 许晨霞. ω-3/6多不饱和脂肪酸与儿童肥胖的两样本孟德尔随机化研究[J]. 中国儿童保健杂志, 2025, 33(8): 841-847.
[3]	王烨妍, 王景刚, 郜莉, 郑浩轩, 陈永强, 曹建国. 儿童肥胖症运动干预研究进展[J]. 中国儿童保健杂志, 2025, 33(8): 878-882.
[4]	王飞英, 秦宏超, 陶小冬, 瞿秋婵, 倪勇, 许占斌. 孤独症谱系障碍儿童超重/肥胖现况及其与情绪行为问题的相关性[J]. 中国儿童保健杂志, 2025, 33(7): 729-732.
[5]	王韵, 曾霞. 睡眠时长和久坐行为对儿童青少年超重肥胖的联合作用[J]. 中国儿童保健杂志, 2025, 33(5): 514-519.
[6]	方雯, 李琴, 程梦晗, 傅晔, 张苗, 逯雨. 小学生睡眠时间和视屏时间与超重肥胖的关联[J]. 中国儿童保健杂志, 2025, 33(5): 549-554.
[7]	魏雨萌, 杨凡. 孕期咖啡因暴露对儿童生长发育影响的研究进展[J]. 中国儿童保健杂志, 2025, 33(3): 303-307.
[8]	洪烨, 傅君芬. 中国儿童肥胖健康报告与防控策略[J]. 中国儿童保健杂志, 2025, 33(2): 117-126.
[9]	周誉, 王海俊. 肥胖儿童的运动干预[J]. 中国儿童保健杂志, 2025, 33(2): 127-131.
[10]	刘璐洁, 徐东, 肖延风, 尹春燕. 肥胖伴非酒精性脂肪肝儿童的血清脂质代谢特征[J]. 中国儿童保健杂志, 2025, 33(2): 136-141.
[11]	严诗钰, 刘沂, 殷丽, 张莉, 段雪霞, 梁滨, 李燕, 王海俊. 山东省两城市学龄前儿童肥胖的影响因素[J]. 中国儿童保健杂志, 2025, 33(2): 142-148.
[12]	程国栋, 朱琳, 秦煜玲. 不同减重量对肥胖儿童青少年非酒精性脂肪肝病的改善作用[J]. 中国儿童保健杂志, 2025, 33(2): 149-154.
[13]	秦煜玲, 朱琳, 程国栋. 减重率与肥胖青少年静息代谢率变化量的剂量-效应关系研究[J]. 中国儿童保健杂志, 2025, 33(2): 155-159.
[14]	何璐, 赵焱, 龚金鑫, 赵璐, 张小林, 毛广惠, 马周瑞, 师晓燕, 蔡世忠, 严向明. 基于体成分探索儿童体脂状况及适宜的肥胖界值点[J]. 中国儿童保健杂志, 2025, 33(2): 160-165.
[15]	杨喆, 张浩, 张海悦, 梁英, 王玥, 张薇, 张玉海, 尚磊. 基于网络分析的学龄前儿童饮食行为和喂养行为与体重的相关性研究[J]. 中国儿童保健杂志, 2025, 33(2): 166-172.