脂质代谢重编程在代谢相关脂肪性肝病进展中的作用机制

程新月; 罗磊; 刘熔; 曹帅兵; 禄保平

doi:10.12449/JCH260923

脂质代谢重编程在代谢相关脂肪性肝病进展中的作用机制

DOI: 10.12449/JCH260923

程新月¹,
罗磊²,
刘熔¹,
曹帅兵¹,
禄保平^{1, 3, , ,}

1.
河南中医药大学第二临床医学院，郑州 450046
2.
河南省中医院（河南中医药大学第二附属医院），郑州 450002
3.
河南中医药大学肝病研究所，郑州 450046

基金项目:

国家自然科学基金 (82305074);

河南省中医药科学研究专项课题 (2024ZY2156);

河南省中医药科学研究专项课题 (2025ZY1031);

河南省科技攻关项目 (262102310449)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：程新月负责撰写论文；罗磊负责课题设计及修改论文；刘熔、曹帅兵负责文献检索及整理；禄保平负责拟定写作思路及最后定稿。

详细信息

通信作者:
禄保平， lbp1921@sohu.com （ORCID： 0000-0002-3707-2185）

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出版历程
- 收稿日期: 2026-01-11
- 录用日期: 2026-03-20
- 出版日期: 2026-09-25

Mechanism of action of lipid metabolic reprogramming in the progression of metabolic dysfunction-associated fatty liver disease

1.
The Second Clinical Medical College of Henan University of Chinese Medicine，Zhengzhou 450046，China
2.
Henan Province Hospital of Traditional Chinese Medicine （The Second Affiliated Hospital of Henan University of Chinese Medicine），Zhengzhou 450002，China
3.
Institute of Liver Diseases，Henan University of Chinese Medicine，Zhengzhou 450046，China

Research funding:

National Natural Science Foundation of China (82305074);

Special Project for Traditional Chinese Medicine Research of Henan Province (2024ZY2156);

Special Project for Traditional Chinese Medicine Research of Henan Province (2025ZY1031);

Henan Key Research and Development Program (262102310449)

More Information

Corresponding author: Lu Baoping， lbp1921@sohu.com （ORCID： 0000-0002-3707-2185）

摘要

摘要: 代谢相关脂肪性肝病（MAFLD）是全球患病率最高的慢性肝病，其疾病谱涵盖从肝脂肪变性到代谢相关脂肪性肝炎、肝纤维化、肝硬化及肝细胞癌的演进过程。近年来，MAFLD的研究范式已从“脂质堆积”转向“脂质代谢重编程”，其作为疾病发生进展的关键环节，受多维度分子网络调控。本综述系统梳理MAFLD中脂质代谢重编程的分子机制：解析脂质代谢紊乱的核心作用，重点阐述内质网-线粒体接触等细胞器互作失调的介导作用；聚焦脂毒性诱发的铁死亡等新型程序性细胞死亡，揭示其加剧肝损伤的通路；整合腺苷一磷酸活化的蛋白质激酶、核转录因子红系2相关因子2等关键信号通路的调控网络，探讨液-液相分离、微蛋白调控等新兴机制。展望了靶向脂质代谢重编程关键节点的潜在治疗策略，为MAFLD的病理机制研究及精准干预提供理论依据。
- 脂质代谢重编程 /
- 代谢相关脂肪性肝病 /
- 代谢相关脂肪性肝炎 /
- 脂肪酸类
Abstract: Metabolic dysfunction-associated fatty liver disease （MAFLD） is the chronic liver disease with the highest prevalence rate globally， and its disease spectrum encompasses a progressive continuum from hepatic steatosis to metabolic dysfunction-associated steatohepatitis， liver fibrosis， liver cirrhosis， and eventually hepatocellular carcinoma. In recent years， the research paradigm of MAFLD has shifted from “lipid accumulation” to “lipid metabolic reprogramming”， which， as a critical link in disease development and progression， is regulated by multidimensional molecular networks. This article systematically reviews the molecular mechanisms of lipid metabolic reprogramming in MAFLD from the following aspects： it analyzes the core role of lipid metabolism disorders， with a focus on how dysregulation of membranous organelle interactions， such as endoplasmic reticulum-mitochondria contacts， mediates metabolic imbalance； it concentrates on novel programmed cell death pathways induced by lipotoxicity， especially ferroptosis， and reveals the pathways through which they exacerbate liver injury； furthermore， it comprehensively analyzes the multi-layered regulatory network of the key signaling pathways such as adenosine monophosphate-activated protein kinase and nuclear factor-erythroid 2-related factor 2 and explores the emerging mechanisms such as liquid-liquid phase separation and microprotein regulation； finally， it provides an outlook on the potential therapeutic strategies targeting critical nodes of lipid metabolic reprogramming， so as to provide a theoretical basis for investigating the pathological mechanisms of MAFLD and developing precise interventions.
- Lipid Metabolic Reprogramming /
- Metabolic Dysfunction-Associated Fatty Liver Disease /
- Metabolic Dysfunction-Associated Steatohepatitis /
- Fatty Acids

HTML全文

注： MAFLD，代谢相关脂肪性肝病；AMPK，腺苷一磷酸活化的蛋白质激酶；Nrf2，核转录因子红系2相关因子2；p38/MAPK，p38丝裂原活化蛋白激酶；JAK/STAT，Janus激酶/信号转导与转录激活因子；Cidec，细胞死亡诱导DFFA样效应蛋白C；UFD1s，剪接体泛素融合降解蛋白1样蛋白。

图 1 MAFLD脂质代谢重编程与病理机制概览

Figure 1. Overview of lipid metabolism reprogramming and pathological mechanisms in MAFLD

下载: 全尺寸图片幻灯片

参考文献(67)

[1]	Rios R S, Zheng K I, Zheng M H. Non-alcoholic steatohepatitis and risk of hepatocellular carcinoma[J]. Chin Med J, 2021, 134( 24): 2911- 2921. DOI: 10.1097/CM9.0000000000001888.
[2]	Teng M L, Ng C H, Huang D Q, et al. Global incidence and prevalence of nonalcoholic fatty liver disease[J]. Clin Mol Hepatol, 2023, 29( Suppl): S32- S42. DOI: 10.3350/cmh.2022.0365.
[3]	Loomba R, Friedman S L, Shulman G I. Mechanisms and disease consequences of nonalcoholic fatty liver disease[J]. Cell, 2021, 184( 10): 2537- 2564. DOI: 10.1016/j.cell.2021.04.015.
[4]	Buzzetti E, Pinzani M, Tsochatzis E A. The multiple-hit pathogenesis of non-alcoholic fatty liver disease(NAFLD)[J]. Metabolism, 2016, 65( 8): 1038- 1048. DOI: 10.1016/j.metabol.2015.12.012.
[5]	Anwar S D, Foster C, Ashraf A. Lipid disorders and metabolic-associated fatty liver disease[J]. Endocrinol Metab Clin North Am, 2023, 52( 3): 445- 457. DOI: 10.1016/j.ecl.2023.01.003.
[6]	Heeren J, Scheja L. Metabolic-associated fatty liver disease and lipoprotein metabolism[J]. Mol Metab, 2021, 50: 101238. DOI: 10.1016/j.molmet.2021.101238.
[7]	Min Yiyang, Zhang Peng, Tian Peirong, et al. The mechanism of bariatric surgery in the treatment of non-alcoholic fatty liver disease[J]. Chin J Dig Surg, 2024, 23( 9): 1231- 1236. DOI: 10.3760/cma.j.cn115610-20240614-00296. 闵逸洋, 张鹏, 田沛荣, 等. 减重手术治疗非酒精性脂肪性肝病的作用机制[J]. 中华消化外科杂志, 2024, 23( 9): 1231- 1236. DOI: 10.3760/cma.j.cn115610-20240614-00296.
[8]	Tanase D M, Gosav E M, Costea C F, et al. The intricate relationship between type 2 diabetes mellitus(T2DM), insulin resistance(IR), and nonalcoholic fatty liver disease(NAFLD)[J]. J Diabetes Res, 2020, 2020: 3920196. DOI: 10.1155/2020/3920196.
[9]	Esler W P, Cohen D E. Pharmacologic inhibition of lipogenesis for the treatment of NAFLD[J]. J Hepatol, 2024, 80( 2): 362- 377. DOI: 10.1016/j.jhep.2023.10.042.
[10]	Zeng H, Qin H, Liao M, et al. CD36 promotes de novo lipogenesis in hepatocytes through INSIG2-dependent SREBP1 processing[J]. Mol Metab, 2022, 57: 101428. DOI: 10.1016/j.molmet.2021.101428.
[11]	Régnier M, Carbinatti T, Parlati L, et al. The role of ChREBP in carbohydrate sensing and NAFLD development[J]. Nat Rev Endocrinol, 2023, 19( 6): 336- 349. DOI: 10.1038/s41574-023-00809-4.
[12]	Ferré P, Phan F, Foufelle F. SREBP-1c and lipogenesis in the liver: An update1[J]. Biochem J, 2021, 478( 20): 3723- 3739. DOI: 10.1042/BCJ20210071.
[13]	Zhao Y, Zhou Y N, Wang D, et al. Mitochondrial dysfunction in metabolic dysfunction fatty liver disease(MAFLD)[J]. Int J Mol Sci, 2023, 24( 24): 17514. DOI: 10.3390/ijms242417514.
[14]	Zhong J, He X F, Gao X X, et al. Hyodeoxycholic acid ameliorates nonalcoholic fatty liver disease by inhibiting RAN-mediated PPARα nucleus-cytoplasm shuttling[J]. Nat Commun, 2023, 14( 1): 5451. DOI: 10.1038/s41467-023-41061-8.
[15]	Liang K. Mitochondrial CPT1A: Insights into structure, function, and basis for drug development[J]. Front Pharmacol, 2023, 14: 1160440. DOI: 10.3389/fphar.2023.1160440.
[16]	Ghosh S S, Wang J, Ghosh S. Measurement of in vivo VLDL and chylomicron secretion[J]. Methods Mol Biol, 2022, 2455: 63- 71. DOI: 10.1007/978-1-0716-2128-8_6.
[17]	Wei H S, Wei H L, Zhao F, et al. Glycosyltransferase GLT8D2 positively regulates ApoB100 protein expression in hepatocytes[J]. Int J Mol Sci, 2013, 14( 11): 21435- 21446. DOI: 10.3390/ijms141121435.
[18]	Sharma S, Kabeer S W, Kumar V, et al. Adiponectin receptor agonist, AdipoRon, restores hepatic clock gene expression in PCOS-associated NAFLD[J]. Sci Rep, 2025, 15( 1): 33729. DOI: 10.1038/s41598-025-93126-x.
[19]	Petrescu M, Vlaicu S I, Ciumărnean L, et al. Chronic inflammation: A link between nonalcoholic fatty liver disease(NAFLD) and dysfunctional adipose tissue[J]. Medicina, 2022, 58( 5): 641. DOI: 10.3390/medicina58050641.
[20]	Kumar G, Shah Y R, Shahzad A, et al. Genetic predeterminants and recent advancements in steatotic liver disease: A roadmap toward precision hepatology[J]. World J Hepatol, 2025, 17( 11): 111576. DOI: 10.4254/wjh.v17.i11.111576.
[21]	Marchisello S, Di Pino A, Scicali R, et al. Pathophysiological, molecular and therapeutic issues of nonalcoholic fatty liver disease: An overview[J]. Int J Mol Sci, 2019, 20( 8): 1948. DOI: 10.3390/ijms20081948.
[22]	Hao J W, Wang J, Guo H L, et al. CD36 facilitates fatty acid uptake by dynamic palmitoylation-regulated endocytosis[J]. Nat Commun, 2020, 11( 1): 4765. DOI: 10.1038/s41467-020-18565-8.
[23]	Martin K, Hatab A, Athwal V S, et al. Genetic contribution to non-alcoholic fatty liver disease and prognostic implications[J]. Curr Diabetes Rep, 2021, 21( 3): 8. DOI: 10.1007/s11892-021-01377-5.
[24]	Zhou M, Lv J Y, Chen X L, et al. From gut to liver: Exploring the crosstalk between gut-liver axis and oxidative stress in metabolic dysfunction-associated steatotic liver disease[J]. Ann Hepatol, 2025, 30( 1): 101777. DOI: 10.1016/j.aohep.2025.101777.
[25]	Buchynskyi M, Kamyshna I, Halabitska I, et al. Unlocking the gut-liver axis: Microbial contributions to the pathogenesis of metabolic-associated fatty liver disease[J]. Front Microbiol, 2025, 16: 1577724. DOI: 10.3389/fmicb.2025.1577724.
[26]	Harned T C, Stan R V, Cao Z, et al. Acute ACAT1/SOAT1 blockade increases MAM cholesterol and strengthens ER-mitochondria connectivity[J]. Int J Mol Sci, 2023, 24( 6): 5525. DOI: 10.3390/ijms24065525.
[27]	Hernández-Alvarez M I, Sebastián D, Vives S, et al. Deficient endoplasmic reticulum-mitochondrial phosphatidylserine transfer causes liver disease[J]. Cell, 2019, 177( 4): 881- 895. DOI: 10.1016/j.cell.2019.04.010.
[28]	Bassot A, Prip-Buus C, Alves A, et al. Loss and gain of function of Grp75 or mitofusin 2 distinctly alter cholesterol metabolism, but all promote triglyceride accumulation in hepatocytes[J]. Biochim Biophys Acta BBA Mol Cell Biol Lipds, 2021, 1866( 12): 159030. DOI: 10.1016/j.bbalip.2021.159030.
[29]	Dewidar B, Mastrototaro L, Englisch C, et al. Alterations of hepatic energy metabolism in murine models of obesity, diabetes and fatty liver diseases[J]. EBioMedicine, 2023, 94: 104714. DOI: 10.1016/j.ebiom.2023.104714.
[30]	Wei X J, Fu Y X, Fang Y, et al. Hepatocyte RAP1A deletion impairs lipid catabolism and worsens steatosis via autophagy activation[J]. Diabetes Metab J, 2025. DOI: 10.4093/dmj.2025.0388.[ Epub ahead of print]
[31]	Mashek D G. Hepatic lipid droplets: A balancing act between energy storage and metabolic dysfunction in NAFLD[J]. Mol Metab, 2021, 50: 101115. DOI: 10.1016/j.molmet.2020.101115.
[32]	Olzmann J A, Carvalho P. Dynamics and functions of lipid droplets[J]. Nat Rev Mol Cell Biol, 2019, 20( 3): 137- 155. DOI: 10.1038/s41580-018-0085-z.
[33]	Lyu X C, Wang J, Wang J Q, et al. A gel-like condensation of Cidec generates lipid-permeable plates for lipid droplet fusion[J]. Dev Cell, 2021, 56( 18): 2592- 2606. DOI: 10.1016/j.devcel.2021.08.015.
[34]	Scorletti E, Carr R M. A new perspective on NAFLD: Focusing on lipid droplets[J]. J Hepatol, 2022, 76( 4): 934- 945. DOI: 10.1016/j.jhep.2021.11.009.
[35]	Ajoolabady A, Kaplowitz N, Lebeaupin C, et al. Endoplasmic reticulum stress in liver diseases[J]. Hepatology, 2023, 77( 2): 619- 639. DOI: 10.1002/hep.32562.
[36]	van Vliet A R, Agostinis P. Mitochondria-associated membranes and ER stress[J]. Curr Top Microbiol Immunol, 2018, 414: 73- 102. DOI: 10.1007/82_2017_2.
[37]	Zhao W J, Wang X Y, Nie W L, et al. Zhimu-Huangbai herb-pair ameliorates hepatic steatosis in mice by regulating IRE1α/XBP1s pathway to inhibit SREBP-1c[J]. Phytomedicine, 2024, 134: 156017. DOI: 10.1016/j.phymed.2024.156017.
[38]	Cláudio N, Dalet A, Gatti E, et al. Mapping the crossroads of immune activation and cellular stress response pathways[J]. EMBO J, 2013, 32( 9): 1214- 1224. DOI: 10.1038/emboj.2013.80.
[39]	Ceja-Galicia Z A, Cespedes-Acuña C L A, El-Hafidi M. Protection strategies against palmitic acid-induced lipotoxicity in metabolic syndrome and related diseases[J]. Int J Mol Sci, 2025, 26( 2): 788. DOI: 10.3390/ijms26020788.
[40]	Ye L Y, Zhao D, Xu Y Z, et al. LncRNA-Gm9795 promotes inflammation in non-alcoholic steatohepatitis via NF-κB/JNK pathway by endoplasmic reticulum stress[J]. J Transl Med, 2021, 19( 1): 101. DOI: 10.1186/s12967-021-02769-7.
[41]	Gao Yiyun, Zhan Xinyu, Zhou Haoming. The role of endoplasmic reticulum stress in regulating macrophage immune response in liver diseases[J]. Organ Transplant, 2024, 15( 6): 889- 894. DOI: 10.3969/j.issn.1674-7445.2024144. 高逸云, 詹欣雨, 周浩明. 内质网应激调控巨噬细胞免疫应答在肝脏疾病中的作用[J]. 器官移植, 2024, 15( 6): 889- 894. DOI: 10.3969/j.issn.1674-7445.2024144.
[42]	Yazıcı D, Sezer H. Insulin resistance, obesity and lipotoxicity[J]. Adv Exp Med Biol, 2017, 960: 277- 304. DOI: 10.1007/978-3-319-48382-5_12.
[43]	Akhter N, Wilson A, Arefanian H, et al. Endoplasmic reticulum stress promotes the expression of TNF-α in THP-1 cells by mechanisms involving ROS/CHOP/HIF-1α and MAPK/NF-κB pathways[J]. Int J Mol Sci, 2023, 24( 20): 15186. DOI: 10.3390/ijms242015186.
[44]	Paul B, Lewinska M, Andersen J B. Lipid alterations in chronic liver disease and liver cancer[J]. JHEP Rep, 2022, 4( 6): 100479. DOI: 10.1016/j.jhepr.2022.100479.
[45]	Dixon S J, Olzmann J A. The cell biology of ferroptosis[J]. Nat Rev Mol Cell Biol, 2024, 25( 6): 424- 442. DOI: 10.1038/s41580-024-00703-5.
[46]	El-Naby S M A, Khedr N F, El-Ashmawy N E, et al. Proanthocyanidin and mitoglitazone suppress lipogenesis by targeting ferroptosis in metabolic dysfunction-associated steatohepatitis[J]. Naunyn Schmiedebergs Arch Pharmacol, 2025, 398( 11): 15825- 15836. DOI: 10.1007/s00210-025-04271-z.
[47]	Tsurusaki S, Tsuchiya Y, Koumura T, et al. Hepatic ferroptosis plays an important role as the trigger for initiating inflammation in nonalcoholic steatohepatitis[J]. Cell Death Dis, 2019, 10: 449. DOI: 10.1038/s41419-019-1678-y.
[48]	Li S X, Zhang Y X, Li P P, et al. IL-22 attenuates MAFLD progression by modulating oxidative stress and ferroptosis[J]. Sci Rep, 2025, 15( 1): 45166. DOI: 10.1038/s41598-025-28718-8.
[49]	Li X Z, Wang X L, Liu X, et al. A UFD1 variant encoding a microprotein modulates UFD1f and IPMK ubiquitination to play pivotal roles in anti-stress responses[J]. Nat Commun, 2025, 16: 6695. DOI: 10.1038/s41467-025-62073-6.
[50]	Ezquerro S, Mocha F, Frühbeck G, et al. Ghrelin reduces TNF-α-induced human hepatocyte apoptosis, autophagy, and pyroptosis: Role in obesity-associated NAFLD[J]. J Clin Endocrinol Metab, 2019, 104( 1): 21- 37. DOI: 10.1210/jc.2018-01171.
[51]	Dong J, Li M Z, Peng R S, et al. ACACA reduces lipid accumulation through dual regulation of lipid metabolism and mitochondrial function via AMPK- PPARα- CPT1A axis[J]. J Transl Med, 2024, 22( 1): 196. DOI: 10.1186/s12967-024-04942-0.
[52]	Shi Qian, Ran Suye, Song Lingyu, et al. NLRP6 overexpression improves nonalcoholic fatty liver disease by promoting lipid oxidation and decomposition in hepatocytes through the AMPK/CPT1A/PGC1A pathway[J]. J Southern Med Univ, 2025, 45( 1): 118- 125. DOI: 10.12122/j.issn.1673-4254.2025.01.15. 石情, 冉苏叶, 宋铃榆, 等. NLRP6过表达通过AMPK/CPT1A/PGC1A通路促进肝细胞脂肪氧化分解改善非酒精性脂肪肝[J]. 南方医科大学学报, 2025, 45( 1): 118- 125. DOI: 10.12122/j.issn.1673-4254.2025.01.15
[53]	Lee J, Kim S, Ju Y, et al. KN21, a direct AMPK activator, alleviates hepatic steatosis and fibrosis by modulating long-chain TAG and pyrimidine metabolism in a MASH mouse model[J]. Biomed Pharmacother, 2025, 193: 118798. DOI: 10.1016/j.biopha.2025.118798.
[54]	Donohoe F, Wilkinson M, Baxter E, et al. Mitogen-activated protein kinase(MAPK) and obesity-related cancer[J]. Int J Mol Sci, 2020, 21( 4): 1241. DOI: 10.3390/ijms21041241.
[55]	Hu X Y, li J, Fu M R, et al. The JAK/STAT signaling pathway: From bench to clinic[J]. Sig Transduct Target Ther, 2021, 6: 402. DOI: 10.1038/s41392-021-00791-1.
[56]	Gong X W, Xu Y J, Yang Q H, et al. Effect of soothing Gan(liver) and invigorating pi(spleen) recipes on TLR4-p38 MAPK pathway in kupffer cells of non-alcoholic steatohepatitis rats[J]. Chin J Integr Med, 2019, 25( 3): 216- 224. DOI: 10.1007/s11655-018-2829-6.
[57]	Deng Y J, Tang K R, Chen R S, et al. Effects of Shugan-Jianpi recipe on the expression of the p38 MAPK/NF-κB signaling pathway in the hepatocytes of NAFLD rats[J]. Medicines(Basel), 2018, 5( 3): 106. DOI: 10.3390/medicines5030106.
[58]	Wang F X, Zhang X, Liu W X, et al. Activated natural killer cell promotes nonalcoholic steatohepatitis through mediating JAK/STAT pathway[J]. Cell Mol Gastroenterol Hepatol, 2022, 13( 1): 257- 274. DOI: 10.1016/j.jcmgh.2021.08.019.
[59]	Bellezza I, Giambanco I, Minelli A, et al. Nrf2-Keap1 signaling in oxidative and reductive stress[J]. Biochim Biophys Acta Mol Cell Res, 2018, 1865( 5): 721- 733. DOI: 10.1016/j.bbamcr.2018.02.010.
[60]	Yang K, Yu X X, Guo Z H, et al. PIM1 alleviated liver oxidative stress and NAFLD by regulating the NRF2/HO-1/NQO1 pathway[J]. Life Sci, 2024, 349: 122714. DOI: 10.1016/j.lfs.2024.122714.
[61]	Zhang X, Yin G L, Chen S W, et al. Diosgenin ameliorating non-alcoholic fatty liver disease via Nrf2-mediated regulation of oxidative stress and ferroptosis[J]. Diabetes Obes Metab, 2024, 26( 12): 5745- 5756. DOI: 10.1111/dom.15945.
[62]	Cheng D Y, Zhang M, Zheng Y Z, et al. α-Ketoglutarate prevents hyperlipidemia-induced fatty liver mitochondrial dysfunction and oxidative stress by activating the AMPK-pgc-1α/Nrf2 pathway[J]. Redox Biol, 2024, 74: 103230. DOI: 10.1016/j.redox.2024.103230.
[63]	Wei Y F, zhang Y B, Zhan B H, et al. Asiaticoside alleviated NAFLD by activating Nrf2 and inhibiting the NF-κB pathway[J]. Phytomedicine, 2025, 136: 156317. DOI: 10.1016/j.phymed.2024.156317.
[64]	Li J D, Wang T Q, Liu P P, et al. Hesperetin ameliorates hepatic oxidative stress and inflammation via the PI3K/AKT-Nrf2-ARE pathway in oleic acid-induced HepG2 cells and a rat model of high-fat diet-induced NAFLD[J]. Food Funct, 2021, 12( 9): 3898- 3918. DOI: 10.1039/d0FO02736G.
[65]	Xiao R, Fang J M, Huang Q P, et al. The effect and mechanism of Germacrone in ameliorating alcoholic fatty liver by inhibiting Nrf2/Rbp4[J]. Chin Med, 2025, 20( 1): 77. DOI: 10.1186/s13020-025-01132-y.
[66]	Gupta A, Balakrishnan B, Karki S, et al. Human CIDEC transgene improves lipid metabolism and protects against high-fat diet–induced glucose intolerance in mice[J]. J Biol Chem, 2022, 298( 9): 102347. DOI: 10.1016/j.jbc.2022.102347.
[67]	Ye J, Huang X Y, Yuan M M, et al. HSD17B13 liquid-liquid phase separation promotes leukocyte adhesion in chronic liver inflammation[J]. J Mol Cell Biol, 2024, 16( 6): mjae018. DOI: 10.1093/jmcb/mjae018.