肿瘤坏死因子-α对过氧化物酶体增殖物激活受体γ功能的调节
Regulation of PPARgamma function by TNF-alpha.
作者信息
Ye Jianping
机构信息
Pennington Biomedical Research Center, Louisiana State University System, 6400 Perkins Road, Baton Rouge, LA 70808, USA.
出版信息
Biochem Biophys Res Commun. 2008 Sep 26;374(3):405-8. doi: 10.1016/j.bbrc.2008.07.068. Epub 2008 Jul 23.
Abstract
The nuclear receptor PPARgamma is a lipid sensor that regulates lipid metabolism through gene transcription. Inhibition of PPARgamma activity by TNF-alpha is involved in pathogenesis of insulin resistance, atherosclerosis, inflammation, and cancer cachexia. PPARgamma activity is regulated by TNF-alpha at pre-translational and post-translational levels. Activation of serine kinases including IKK, ERK, JNK, and p38 may be involved in the TNF-regulation of PPARgamma. Of the four kinases, IKK is a dominant signaling molecule in the TNF-regulation of PPARgamma. IKK acts through at least two mechanisms: inhibition of PPARgamma expression and activation of PPARgamma corepressor. In this review article, literature is reviewed with a focus on the mechanisms of PPARgamma inhibition by TNF-alpha.
摘要
核受体PPARγ是一种脂质传感器，通过基因转录调节脂质代谢。肿瘤坏死因子-α（TNF-α）对PPARγ活性的抑制作用与胰岛素抵抗、动脉粥样硬化、炎症及癌症恶病质的发病机制有关。PPARγ活性在翻译前和翻译后水平均受到TNF-α的调节。包括IKK、ERK、JNK和p38在内的丝氨酸激酶的激活可能参与了TNF对PPARγ的调节。在这四种激酶中，IKK是TNF调节PPARγ过程中的主要信号分子。IKK至少通过两种机制发挥作用：抑制PPARγ表达和激活PPARγ共抑制因子。在这篇综述文章中，我们将重点回顾关于TNF-α抑制PPARγ机制的相关文献。
相似文献
1
Regulation of PPARgamma function by TNF-alpha.肿瘤坏死因子-α对过氧化物酶体增殖物激活受体γ功能的调节
Biochem Biophys Res Commun. 2008 Sep 26;374(3):405-8. doi: 10.1016/j.bbrc.2008.07.068. Epub 2008 Jul 23.
2
Regulation of nuclear translocation of HDAC3 by IkappaBalpha is required for tumor necrosis factor inhibition of peroxisome proliferator-activated receptor gamma function.IkappaBalpha对HDAC3核转位的调节是肿瘤坏死因子抑制过氧化物酶体增殖物激活受体γ功能所必需的。
J Biol Chem. 2006 Feb 17;281(7):4540-7. doi: 10.1074/jbc.M507784200. Epub 2005 Dec 21.
3
Hypertension-Causing Mutation in Peroxisome Proliferator-Activated Receptor γ Impairs Nuclear Export of Nuclear Factor-κB p65 in Vascular Smooth Muscle.过氧化物酶体增殖物激活受体γ中的高血压致病突变损害血管平滑肌中核因子κB p65的核输出。
Hypertension. 2017 Jul;70(1):174-182. doi: 10.1161/HYPERTENSIONAHA.117.09276. Epub 2017 May 15.
4
15-deoxy-Δ(12,14) -prostaglandin-J2 and ciglitazone inhibit TNF-α-induced matrix metalloproteinase 13 production via the antagonism of NF-κB activation in human synovial fibroblasts.15-脱氧-Δ(12,14)-前列腺素 J2 和西格列酮通过拮抗 NF-κB 活化抑制 TNF-α诱导的人滑膜成纤维细胞基质金属蛋白酶 13 的产生。
J Cell Physiol. 2011 Dec;226(12):3242-50. doi: 10.1002/jcp.22685.
5
Selective deletion of adipocytes, but not preadipocytes, by TNF-alpha through C/EBP- and PPARgamma-mediated suppression of NF-kappaB.肿瘤坏死因子-α通过 C/EBP 和 PPARγ 介导的核因子-κB 抑制作用选择性地删除脂肪细胞，但不删除前脂肪细胞。
Lab Invest. 2010 Sep;90(9):1385-95. doi: 10.1038/labinvest.2010.118. Epub 2010 Jun 21.
6
Effect of Salusin-β on Peroxisome Proliferator-Activated Receptor Gamma Gene Expression in Vascular Smooth Muscle Cells and its Possible Mechanism.Salusin-β对血管平滑肌细胞中过氧化物酶体增殖物激活受体γ基因表达的影响及其可能机制
Cell Physiol Biochem. 2015;36(6):2466-79. doi: 10.1159/000430207. Epub 2015 Aug 10.
7
Opposite action of peroxisome proliferator-activated receptor-gamma in regulating renal inflammation: functional switch by its ligand.过氧化物酶体增殖物激活受体-γ在调节肾脏炎症中的相反作用：配体的功能转换。
J Biol Chem. 2010 Sep 24;285(39):29981-8. doi: 10.1074/jbc.M110.110908. Epub 2010 Jul 27.
8
Peroxisome proliferator-activated receptor activity is involved in the osteoblastic differentiation regulated by bone morphogenetic proteins and tumor necrosis factor-α.过氧化物酶体增殖物激活受体活性参与骨形态发生蛋白和肿瘤坏死因子-α调节的成骨细胞分化。
Mol Cell Endocrinol. 2012 Jan 2;348(1):224-32. doi: 10.1016/j.mce.2011.08.027. Epub 2011 Aug 25.
9
Peptidoglycan induced expression of peroxisome proliferator-activated receptor γ in mouse peritoneal macrophages: role of ERK and JNK MAP kinases.肽聚糖诱导小鼠腹腔巨噬细胞过氧化物酶体增殖物激活受体 γ 的表达：ERK 和 JNK MAP 激酶的作用。
Cytokine. 2012 Dec;60(3):778-86. doi: 10.1016/j.cyto.2012.07.036. Epub 2012 Aug 25.
10
PPARγ as a molecular target of EPA anti-inflammatory activity during TNF-α-impaired skeletal muscle cell differentiation.PPARγ 作为 EPA 抑制 TNF-α诱导的成肌细胞分化过程中抗炎活性的分子靶标
J Nutr Biochem. 2012 Nov;23(11):1440-8. doi: 10.1016/j.jnutbio.2011.09.005. Epub 2012 Feb 2.
引用本文的文献
1
Metabolic challenges of glucose and lipid dysregulation in psoriatic arthritis: a narrative review from pathogenesis to clinical practice.银屑病关节炎中葡萄糖和脂质代谢失调的代谢挑战：从发病机制到临床实践的叙述性综述
Acta Diabetol. 2025 Aug 14. doi: 10.1007/s00592-025-02565-5.
2
Andrographolide Mitigates Inflammation and Reverses UVB-Induced Metabolic Reprogramming in HaCaT Cells.穿心莲内酯减轻HaCaT细胞中的炎症并逆转紫外线B诱导的代谢重编程。
Int J Mol Sci. 2025 Jul 6;26(13):6508. doi: 10.3390/ijms26136508.
3
Clinical and Experimental Insights into the Role of NETosis in IgA Nephropathy Pathogenesis.关于中性粒细胞胞外诱捕网形成在IgA肾病发病机制中作用的临床与实验见解
Kidney Dis (Basel). 2025 May 9;11(1):450-468. doi: 10.1159/000546343. eCollection 2025 Jan-Dec.
4
Pig models reveal the interplay between fatty acids and cytokines in skeletal muscle.猪模型揭示了骨骼肌中脂肪酸与细胞因子之间的相互作用。
Sci Rep. 2025 Jun 4;15(1):19528. doi: 10.1038/s41598-025-04273-0.
5
Brain insulin resistance mediated cognitive impairment and neurodegeneration: Type-3 diabetes or Alzheimer's Disease.脑胰岛素抵抗介导的认知障碍和神经退行性变：3型糖尿病还是阿尔茨海默病。
Acta Neurol Belg. 2025 Jan 7. doi: 10.1007/s13760-024-02706-7.
6
The dichotomic role of cytokines in aging.细胞因子在衰老过程中的双重作用。
Biogerontology. 2024 Dec 2;26(1):17. doi: 10.1007/s10522-024-10152-4.
7
Effects of d-allose on anti-brain edema effects and reduction of tumor necrosis factor-alpha and interleukin-6 in the water intoxication model.D-阿洛酮糖对水中毒模型抗脑水肿作用及肿瘤坏死因子-α和白细胞介素-6降低的影响。
Heliyon. 2024 May 6;10(10):e30700. doi: 10.1016/j.heliyon.2024.e30700. eCollection 2024 May 30.
8
Review of the direct and indirect effects of hyperglycemia on the HPA axis in T2DM and the co-occurrence of depression.综述 2 型糖尿病患者高血糖对 HPA 轴的直接和间接影响及与抑郁共病的关系。
BMJ Open Diabetes Res Care. 2024 Feb 27;12(1):e003218. doi: 10.1136/bmjdrc-2022-003218.
9
Improvement of Vascular Insulin Sensitivity by Ranolazine.雷诺嗪改善血管胰岛素敏感性。
Int J Mol Sci. 2023 Aug 31;24(17):13532. doi: 10.3390/ijms241713532.
10
PPAR-γ Agonist GW1929 Targeted to Macrophages with Dendrimer-Graphene Nanostars Reduces Liver Fibrosis and Inflammation.用树枝状大分子-石墨烯纳米星靶向巨噬细胞的PPAR-γ激动剂GW1929可减轻肝纤维化和炎症。
Pharmaceutics. 2023 May 10;15(5):1452. doi: 10.3390/pharmaceutics15051452.
本文引用的文献
1
Shared principles in NF-kappaB signaling.核因子κB信号传导中的共同原则。
Cell. 2008 Feb 8;132(3):344-62. doi: 10.1016/j.cell.2008.01.020.
2
Dok1 mediates high-fat diet-induced adipocyte hypertrophy and obesity through modulation of PPAR-gamma phosphorylation.Dok1通过调节PPAR-γ磷酸化介导高脂饮食诱导的脂肪细胞肥大和肥胖。
Nat Med. 2008 Feb;14(2):188-93. doi: 10.1038/nm1706. Epub 2008 Jan 20.
3
Modulation of PPAR activity via phosphorylation.通过磷酸化作用对过氧化物酶体增殖物激活受体（PPAR）活性进行调节。
Biochim Biophys Acta. 2007 Aug;1771(8):952-60. doi: 10.1016/j.bbalip.2007.04.018. Epub 2007 May 22.
4
PPARgamma phosphorylation mediated by JNK MAPK: a potential role in macrophage-derived foam cell formation.由JNK丝裂原活化蛋白激酶介导的PPARγ磷酸化：在巨噬细胞源性泡沫细胞形成中的潜在作用。
Acta Pharmacol Sin. 2006 Sep;27(9):1146-52. doi: 10.1111/j.1745-7254.2006.00359.x.
5
Regulation of nuclear translocation of HDAC3 by IkappaBalpha is required for tumor necrosis factor inhibition of peroxisome proliferator-activated receptor gamma function.IkappaBalpha对HDAC3核转位的调节是肿瘤坏死因子抑制过氧化物酶体增殖物激活受体γ功能所必需的。
J Biol Chem. 2006 Feb 17;281(7):4540-7. doi: 10.1074/jbc.M507784200. Epub 2005 Dec 21.
6
Coactivators and corepressors of NF-kappaB in IkappaB alpha gene promoter.IkappaBα基因启动子中NF-κB的共激活因子和共抑制因子
J Biol Chem. 2005 Jun 3;280(22):21091-8. doi: 10.1074/jbc.M500754200. Epub 2005 Apr 4.
7
SMRT derepression by the IkappaB kinase alpha: a prerequisite to NF-kappaB transcription and survival.IκB激酶α介导的SMRT去抑制：NF-κB转录和细胞存活的前提条件
Mol Cell. 2004 Oct 22;16(2):245-55. doi: 10.1016/j.molcel.2004.10.010.
8
Transcription suppression of peroxisome proliferator-activated receptor gamma2 gene expression by tumor necrosis factor alpha via an inhibition of CCAAT/ enhancer-binding protein delta during the early stage of adipocyte differentiation.在脂肪细胞分化早期，肿瘤坏死因子α通过抑制CCAAT/增强子结合蛋白δ来抑制过氧化物酶体增殖物激活受体γ2基因表达的转录。
Endocrinology. 2004 Nov;145(11):4948-56. doi: 10.1210/en.2004-0180. Epub 2004 Jul 29.
9
Cytoplasmic IkappaBalpha increases NF-kappaB-independent transcription through binding to histone deacetylase (HDAC) 1 and HDAC3.细胞质中的IκBα通过与组蛋白去乙酰化酶（HDAC）1和HDAC3结合增加非NF-κB依赖性转录。
J Biol Chem. 2003 Nov 21;278(47):46541-8. doi: 10.1074/jbc.M306381200. Epub 2003 Sep 12.
10
Troglitazone antagonizes tumor necrosis factor-alpha-induced reprogramming of adipocyte gene expression by inhibiting the transcriptional regulatory functions of NF-kappaB.曲格列酮通过抑制核因子-κB的转录调节功能，拮抗肿瘤坏死因子-α诱导的脂肪细胞基因表达重编程。
J Biol Chem. 2003 Jul 25;278(30):28181-92. doi: 10.1074/jbc.M303141200. Epub 2003 May 5.
Zotero 插件