TWEAK-Fn14 通路：健康与疾病状态下骨骼肌生物学的有力调节者。
The TWEAK-Fn14 pathway: a potent regulator of skeletal muscle biology in health and disease.
机构信息
Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, United States.
Department of Immunology, Biogen Idec, 12 Cambridge Center, Cambridge, MA 02142, United States.
出版信息
Cytokine Growth Factor Rev. 2014 Apr;25(2):215-25. doi: 10.1016/j.cytogfr.2013.12.004. Epub 2013 Dec 24.
Abstract
TNF-like weak inducer of apoptosis (TWEAK), a TNF superfamily ligand, and its bona fide receptor, the TNF receptor superfamily member fibroblast growth factor-inducible 14 (Fn14), represent a pivotal axis for shaping both physiological and pathological tissue responses to acute or chronic injury and disease. In recent years significant advances have been made in delineating the prominent role of TWEAK-Fn14 dyad in regulating skeletal muscle mass and metabolism. Also emerging from the broad study of tissue injury in skeletal muscle and other organs is the role of the TWEAK-Fn14 pathway in promoting fibrosis. This review article highlights recent advancements toward understanding how the TWEAK-Fn14 pathway regulates the response to various skeletal muscle insults and, more broadly, engages multiple mechanisms to drive tissue fibrosis.
摘要
肿瘤坏死因子样弱凋亡诱导因子（TWEAK）是肿瘤坏死因子超家族配体，其真正的受体是肿瘤坏死因子受体超家族成员成纤维细胞生长因子诱导 14（Fn14），它们是调节组织对急性或慢性损伤和疾病的生理和病理反应的关键轴。近年来，在阐明 TWEAK-Fn14 二聚体在调节骨骼肌质量和代谢中的突出作用方面取得了重大进展。从对骨骼肌和其他器官组织损伤的广泛研究中也出现了 TWEAK-Fn14 途径在促进纤维化中的作用。本文综述了近年来在理解 TWEAK-Fn14 途径如何调节各种骨骼肌损伤反应方面的进展，更广泛地说，该途径通过多种机制参与驱动组织纤维化。
相似文献
1
The TWEAK-Fn14 pathway: a potent regulator of skeletal muscle biology in health and disease.TWEAK-Fn14 通路：健康与疾病状态下骨骼肌生物学的有力调节者。
Cytokine Growth Factor Rev. 2014 Apr;25(2):215-25. doi: 10.1016/j.cytogfr.2013.12.004. Epub 2013 Dec 24.
2
TWEAK and TRAF6 regulate skeletal muscle atrophy.TWEAK 和 TRAF6 调节骨骼肌萎缩。
Curr Opin Clin Nutr Metab Care. 2012 May;15(3):233-9. doi: 10.1097/MCO.0b013e328351c3fc.
3
Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.TWEAK-Fn14 信号在骨骼肌萎缩和再生中的争议。
Cell Mol Life Sci. 2020 Sep;77(17):3369-3381. doi: 10.1007/s00018-020-03495-x. Epub 2020 Mar 21.
4
Dysregulation of Tweak and Fn14 in skeletal muscle of spinal muscular atrophy mice.脊髓性肌萎缩症小鼠骨骼肌中 Tweak 和 Fn14 的失调。
Skelet Muscle. 2022 Jul 28;12(1):18. doi: 10.1186/s13395-022-00301-z.
5
TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration.肿瘤坏死因子样弱凋亡诱导因子（TWEAK）通过其受体Fn14，是间充质祖细胞和骨骼肌再生的新型调节因子。
EMBO J. 2006 Dec 13;25(24):5826-39. doi: 10.1038/sj.emboj.7601441. Epub 2006 Nov 23.
6
The TWEAK-Fn14 system: breaking the silence of cytokine-induced skeletal muscle wasting.TWEAK-Fn14 系统：打破细胞因子诱导的骨骼肌消耗的沉默。
Curr Mol Med. 2012 Jan;12(1):3-13. doi: 10.2174/156652412798376107.
7
TWEAK/Fn14 pathway: an immunological switch for shaping tissue responses.TWEAK/Fn14 通路：塑造组织反应的免疫开关。
Immunol Rev. 2011 Nov;244(1):99-114. doi: 10.1111/j.1600-065X.2011.01054.x.
8
The TWEAK-Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice.TWEAK-Fn14 系统是小鼠失神经诱导骨骼肌萎缩的关键调节因子。
J Cell Biol. 2010 Mar 22;188(6):833-49. doi: 10.1083/jcb.200909117.
9
TWEAK/Fn14 pathway is a novel mediator of retinal neovascularization.TWEAK/Fn14 通路是视网膜新生血管的一个新的介导者。
Invest Ophthalmol Vis Sci. 2014 Feb 10;55(2):801-13. doi: 10.1167/iovs.13-12812.
10
The TWEAK-Fn14 dyad is involved in age-associated pathological changes in skeletal muscle.TWEAK-Fn14 二聚体参与骨骼肌与年龄相关的病理变化。
Biochem Biophys Res Commun. 2014 Apr 18;446(4):1219-1224. doi: 10.1016/j.bbrc.2014.03.084. Epub 2014 Mar 26.
引用本文的文献
1
Physical Activity, Exerkines, and Their Role in Cancer Cachexia.体力活动、运动因子及其在癌症恶病质中的作用。
Int J Mol Sci. 2025 Aug 19;26(16):8011. doi: 10.3390/ijms26168011.
2
Sarcopenia: Current Insights into Molecular Mechanisms, Diagnostics, and Emerging Interventional Approaches.肌肉减少症：对分子机制、诊断及新兴干预方法的当前见解
Int J Mol Sci. 2025 Jul 14;26(14):6740. doi: 10.3390/ijms26146740.
3
The TWEAK/Fn14 signaling mediates skeletal muscle wasting during cancer cachexia.TWEAK/Fn14信号传导在癌症恶病质期间介导骨骼肌萎缩。
iScience. 2025 May 30;28(7):112714. doi: 10.1016/j.isci.2025.112714. eCollection 2025 Jul 18.
4
Patients Having Major Abdominal Cancer Surgery Exhibit Significant Acute Muscle Wasting.接受腹部大手术的癌症患者出现明显的急性肌肉萎缩。
J Cachexia Sarcopenia Muscle. 2025 Jun;16(3):e13858. doi: 10.1002/jcsm.13858.
5
Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.成纤维细胞生长因子诱导蛋白14在骨骼肌修复过程中调节卫星细胞的自我更新和增殖。
JCI Insight. 2025 Jan 28;10(5):e187825. doi: 10.1172/jci.insight.187825.
6
Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.成纤维细胞生长因子诱导蛋白14在骨骼肌修复过程中调节卫星细胞的自我更新和增殖。
bioRxiv. 2025 Jan 2:2024.10.06.616900. doi: 10.1101/2024.10.06.616900.
7
The cytokine receptor Fn14 is a molecular brake on neuronal activity that mediates circadian function .细胞因子受体Fn14是神经元活动的分子制动器，可介导昼夜节律功能。
bioRxiv. 2024 Apr 2:2024.04.02.587786. doi: 10.1101/2024.04.02.587786.
8
The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia.巨噬细胞与癌细胞之间的串扰促进胰腺癌恶病质。
Cancer Cell. 2024 May 13;42(5):885-903.e4. doi: 10.1016/j.ccell.2024.03.009. Epub 2024 Apr 11.
9
Exercise microdosing for skeletal muscle health applications to spaceflight.针对航天应用进行骨骼肌健康的运动微剂量研究。
J Appl Physiol (1985). 2024 May 1;136(5):1040-1052. doi: 10.1152/japplphysiol.00491.2023. Epub 2024 Jan 11.
10
Fn14 promotes myoblast fusion during regenerative myogenesis.Fn14 促进再生肌发生过程中的成肌细胞融合。
Life Sci Alliance. 2023 Oct 9;6(12). doi: 10.26508/lsa.202302312. Print 2023 Dec.
本文引用的文献
1
Regulatory circuitry of TWEAK-Fn14 system and PGC-1α in skeletal muscle atrophy program.TWEAK-Fn14 系统和 PGC-1α 在骨骼肌萎缩程序中的调控回路。
FASEB J. 2014 Mar;28(3):1398-411. doi: 10.1096/fj.13-242123. Epub 2013 Dec 10.
2
Proinflammatory cytokine tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) suppresses satellite cell self-renewal through inversely modulating Notch and NF-κB signaling pathways.促炎细胞因子肿瘤坏死因子样凋亡弱诱导剂（TWEAK）通过反向调节 Notch 和 NF-κB 信号通路抑制卫星细胞自我更新。
J Biol Chem. 2013 Dec 6;288(49):35159-69. doi: 10.1074/jbc.M113.517300. Epub 2013 Oct 22.
3
TWEAK promotes exercise intolerance by decreasing skeletal muscle oxidative phosphorylation capacity.TWEAK 通过降低骨骼肌氧化磷酸化能力来促进运动不耐受。
Skelet Muscle. 2013 Jul 8;3(1):18. doi: 10.1186/2044-5040-3-18.
4
Increased expression of atrogenes and TWEAK family members after severe burn injury in nonburned human skeletal muscle.严重烧伤后未烧伤的人体骨骼肌中促萎缩基因和肿瘤坏死因子样弱凋亡诱导因子（TWEAK）家族成员的表达增加。
J Burn Care Res. 2013 Sep-Oct;34(5):e297-304. doi: 10.1097/BCR.0b013e31827a2a9c.
5
The rise of soluble TWEAK levels in severely obese subjects after bariatric surgery may affect adipocyte-cytokine production induced by TNFα.减重手术后严重肥胖患者可溶性 TWEAK 水平的升高可能会影响 TNFα 诱导的脂肪细胞细胞因子产生。
J Clin Endocrinol Metab. 2013 Aug;98(8):E1323-33. doi: 10.1210/jc.2012-4177. Epub 2013 Jun 19.
6
TNF-related weak inducer of apoptosis (TWEAK) promotes kidney fibrosis and Ras-dependent proliferation of cultured renal fibroblast.肿瘤坏死因子相关凋亡弱诱导因子（TWEAK）促进肾纤维化及培养的肾成纤维细胞的Ras依赖性增殖。
Biochim Biophys Acta. 2013 Oct;1832(10):1744-55. doi: 10.1016/j.bbadis.2013.05.032. Epub 2013 Jun 6.
7
Failure of fibrotic liver regeneration in mice is linked to a severe fibrogenic response driven by hepatic progenitor cell activation.纤维化的肝再生失败与肝祖细胞激活驱动的严重纤维生成反应有关。
Am J Pathol. 2013 Jul;183(1):182-94. doi: 10.1016/j.ajpath.2013.03.018. Epub 2013 May 14.
8
Wasting mechanisms in muscular dystrophy.肌肉萎缩症中的消耗机制。
Int J Biochem Cell Biol. 2013 Oct;45(10):2266-79. doi: 10.1016/j.biocel.2013.05.001. Epub 2013 May 11.
9
Protein breakdown in muscle wasting: role of autophagy-lysosome and ubiquitin-proteasome.肌肉消耗中的蛋白质分解：自噬溶酶体和泛素-蛋白酶体的作用。
Int J Biochem Cell Biol. 2013 Oct;45(10):2121-9. doi: 10.1016/j.biocel.2013.04.023. Epub 2013 May 7.
10
Signaling mechanisms in mammalian myoblast fusion.哺乳动物成肌细胞融合中的信号转导机制。
Sci Signal. 2013 Apr 23;6(272):re2. doi: 10.1126/scisignal.2003832.
Zotero 插件