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Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration

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Abstract

Skeletal muscle is one of the largest functional tissues in the human body; it is highly plastic and responds dramatically to anabolic and catabolic stimuli, including weight training and malnutrition, respectively. Excessive loss of muscle mass, or atrophy, is a common symptom of many disease states with severe impacts on prognosis and quality of life. TNF-like weak inducer of apoptosis (TWEAK) and its cognate receptor, fibroblast growth factor-inducible 14 (Fn14) are an emerging cytokine signaling pathway in the pathogenesis of muscle atrophy. Upregulation of TWEAK and Fn14 has been described in a number of atrophic and injured muscle states; however, it remains unclear whether they are contributing to the degenerative or regenerative aspect of muscle insults. The current review focuses on the expression and apparent downstream outcomes of both TWEAK and Fn14 in a range of catabolic and anabolic muscle models. Apparent changes in the signaling outcomes of TWEAK-Fn14 activation dependent on the relative expression of both the ligand and the receptor are discussed as a potential source of divergent TWEAK-Fn14 downstream effects. This review proposes both a physiological and pathological model of TWEAK-Fn14 signaling. Further research is needed on the switch between these states to develop therapeutic interventions for this pathway.

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References

  1. Janssen I, Heymsfield SB, Wang ZM, Ross R (2000) Skeletal muscle mass and distribution in 468 men and women aged 18–88 yr. J Appl Physiol 89(1):81–88

    Article  CAS  Google Scholar 

  2. Jackman RW, Kandarian SC (2004) The molecular basis of skeletal muscle atrophy. Am J Physiol Cell Physiol 287(4):C834–C843. https://doi.org/10.1152/ajpcell.00579.2003

    Article  CAS  PubMed  Google Scholar 

  3. Enwere EK, Lacasse EC, Adam NJ, Korneluk RG (2014) Role of the TWEAK-Fn14-cIAP1-NF-kappaB signaling axis in the regulation of myogenesis and muscle homeostasis. Front Immunol 5:34. https://doi.org/10.3389/fimmu.2014.00034

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Gurunathan S, Winkles JA, Ghosh S, Hayden MS (2014) Regulation of fibroblast growth factor-inducible 14 (Fn14) expression levels via ligand-independent lysosomal degradation. J Biol Chem 289(19):12976–12988. https://doi.org/10.1074/jbc.M114.563478

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Chicheportiche Y, Bourdon PR, Xu H, Hsu YM, Scott H, Hession C, Garcia I, Browning JL (1997) TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis. J Biol Chem 272(51):32401–32410

    Article  CAS  Google Scholar 

  6. Winkles JA (2008) The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targeting. Nat Rev Drug Discov 7(5):411–425. https://doi.org/10.1038/nrd2488

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Chen T, Guo ZP, Li MM, Li JY, Jiao XY, Zhang YH, Liu HJ (2011) Tumour necrosis factor-like weak inducer of apoptosis (TWEAK), an important mediator of endothelial inflammation, is associated with the pathogenesis of Henoch-Schonlein purpura. Clin Exp Immunol 166(1):64–71. https://doi.org/10.1111/j.1365-2249.2011.04442.x

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Nakayama M, Kayagaki N, Yamaguchi N, Okumura K, Yagita H (2000) Involvement of tweak in interferon γ–stimulated monocyte cytotoxicity. J Exp Med 192(9):1373–1380

    Article  CAS  Google Scholar 

  9. Girgenrath M, Weng S, Kostek CA, Browning B, Wang M, Brown SAN, Winkles JA, Michaelson JS, Allaire N, Schneider P, Scott ML, Hsu YM, Yagita H, Flavell RA, Miller JB, Burkly LC, Zheng TS (2006) TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration. EMBO J 25(24):5826–5839. https://doi.org/10.1038/sj.emboj.7601441

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Burkly LC, Michaelson JS, Hahm K, Jakubowski A, Zheng TS (2007) TWEAKing tissue remodeling by a multifunctional cytokine: role of TWEAK/Fn14 pathway in health and disease. Cytokine 40(1):1–16. https://doi.org/10.1016/j.cyto.2007.09.007

    Article  CAS  PubMed  Google Scholar 

  11. Michaelson JS, Cho S, Browning B, Zheng TS, Lincecum JM, Wang MZ, Hsu Y-M, Burkly LC (2005) Tweak induces mammary epithelial branching morphogenesis. Oncogene 24(16):2613–2624. https://doi.org/10.1038/sj.onc.1208208

    Article  CAS  PubMed  Google Scholar 

  12. Blanco-Colio LM, Martin-Ventura JL, Munoz-Garcia B, Orbe J, Paramo JA, Michel JB, Ortiz A, Meilhac O, Egido J (2007) Identification of soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) as a possible biomarker of subclinical atherosclerosis. Arterioscler Thromb Vasc Biol 27(4):916–922. https://doi.org/10.1161/01.ATV.0000258972.10109.ff

    Article  CAS  PubMed  Google Scholar 

  13. Kralisch S, Ziegelmeier M, Bachmann A, Seeger J, Lossner U, Bluher M, Stumvoll M, Fasshauer M (2008) Serum levels of the atherosclerosis biomarker sTWEAK are decreased in type 2 diabetes and end-stage renal disease. Atherosclerosis 199(2):440–444. https://doi.org/10.1016/j.atherosclerosis.2007.10.022

    Article  CAS  PubMed  Google Scholar 

  14. Maymó-Masip E, Vendrell J, Garrifo-Sanchez L, Fernández-Veledo S, Chacón MR, Vázquez-Carballo A, Garcia España A, Tinahones FJ, García-Fuentes E, Rodriguez MdM (2013) The rise of soluble TWEAK levels in severely obese subjects after bariatric surgery may affect adipocyte-cytokine production induced by TNFα. J Clin Endocrinol Metab 98(8):E1323–E1333. https://doi.org/10.1210/jc.2012-4177

    Article  CAS  PubMed  Google Scholar 

  15. Jakubowski A, Ambrose C, Parr M, Lincecum JM, Wang MZ, Zheng TS, Browning B, Michaelson JS, Baetscher M, Wang B, Bissell DM, Burkly LC (2005) TWEAK induces liver progenitor cell proliferation. J Clin Invest 115(9):2330–2340. https://doi.org/10.1172/jci23486

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Zhu C, Zhang L, Liu Z, Li C, Bai Y (2017) TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-kappaB pathway. J Cell Biochem. https://doi.org/10.1002/jcb.26525

    Article  PubMed  PubMed Central  Google Scholar 

  17. Liu J, Peng L, Liu Y, Wu K, Wang S, Wang X, Liu Q, Xia Y, Zeng W (2018) Topical TWEAK accelerates healing of experimental burn wounds in mice. Front Pharmacol 9:660. https://doi.org/10.3389/fphar.2018.00660

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Polek TC, Talpaz M, Darnay BG, Spivak-Kroizman T (2003) TWEAK mediates signal transduction and differentiation of RAW264.7 cells in the absence of Fn14/TweakR. Evidence for a second TWEAK receptor. J Biol Chem 278(34):32317–32323. https://doi.org/10.1074/jbc.M302518200

    Article  CAS  PubMed  Google Scholar 

  19. Xiao G, Lyu M, Wang Y, He S, Liu X, Ni J, Li L, Fan G, Han J, Gao X, Wang X, Zhu Y (2019) Ginkgo flavonol glycosides or ginkgolides tend to differentially protect myocardial or cerebral ischemia-reperfusion injury via regulation of TWEAK-Fn14 signaling in heart and brain. Front Pharmacol 10:735. https://doi.org/10.3389/fphar.2019.00735

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Dogra C, Changotra H, Wedhas N, Qin X, Wergedal JE, Kumar A (2007) TNF-related weak inducer of apoptosis (TWEAK) is a potent skeletal muscle-wasting cytokine. FASEB J 21(8):1857–1869. https://doi.org/10.1096/fj.06-7537com

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Morosetti R, Gliubizzi C, Sancricca C, Broccolini A, Gidaro T, Lucchini M, Mirabella M (2012) TWEAK in inclusion-body myositis muscle: possible pathogenic role of a cytokine inhibiting myogenesis. Am J Pathol 180(4):1603–1613. https://doi.org/10.1016/j.ajpath.2011.12.027

    Article  CAS  PubMed  Google Scholar 

  22. Yadava RS, Foff EP, Yu Q, Gladman JT, Zheng TS, Mahadevan MS (2016) TWEAK regulates muscle functions in a mouse model of RNA toxicity. PLoS ONE 11(2):e0150192. https://doi.org/10.1371/journal.pone.0150192

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Mittal A, Bhatnagar S, Kumar A, Lach-Trifilieff E, Wauters S, Li H, Makonchuk DY, Glass DJ, Kumar A (2010) The TWEAK-Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice. J Cell Biol 188(6):833–849. https://doi.org/10.1083/jcb.200909117

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Wiley SR, Cassiano L, Lofton T, Davis-Smith T, Winkles JA, Lindner V, Liu H, Daniel TO, Smith CA, Fanslow WC (2001) A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis. Immunity 15(5):837–846. https://doi.org/10.1016/S1074-7613(01)00232-1

    Article  CAS  PubMed  Google Scholar 

  25. Chen JL, Walton KL, Winbanks CE, Murphy KT, Thomson RE, Makanji Y, Qian H, Lynch GS, Harrison CA, Gregorevic P (2014) Elevated expression of activins promotes muscle wasting and cachexia. FASEB J 28(4):1711–1723. https://doi.org/10.1096/fj.13-245894

    Article  CAS  PubMed  Google Scholar 

  26. Winer H, Fraiberg M, Abada A, Dadosh T, Tamim-Yecheskel BC, Elazar Z (2018) Autophagy differentially regulates TNF receptor Fn14 by distinct mammalian Atg8 proteins. Nat Commun 9(1):3744. https://doi.org/10.1038/s41467-018-06275-1

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Culp PA, Choi D, Zhang Y, Yin J, Seto P, Ybarra SE, Su M, Sho M, Steinle R, Wong MHL, Evangelista F, Grove J, Cardenas M, James M, Hsi ED, Chao DT, Powers DB, Ramakrishnan V, Dubridge R (2010) Antibodies to TWEAK receptor inhibit human tumor growth through dual mechanisms. Clin Cancer Res 16(2):497–508. https://doi.org/10.1158/1078-0432.ccr-09-1929

    Article  CAS  PubMed  Google Scholar 

  28. Johnston AJ, Murphy KT, Jenkinson L, Laine D, Emmrich K, Faou P, Weston R, Jayatilleke KM, Schloegel J, Talbo G, Casey JL, Levina V, Wong WW, Dillon H, Sahay T, Hoogenraad J, Anderton H, Hall C, Schneider P, Tanzer M, Foley M, Scott AM, Gregorevic P, Liu SY, Burkly LC, Lynch GS, Silke J, Hoogenraad NJ (2015) Targeting of Fn14 prevents cancer-induced cachexia and prolongs survival. Cell 162(6):1365–1378. https://doi.org/10.1016/j.cell.2015.08.031

    Article  CAS  PubMed  Google Scholar 

  29. Wu CL, Kandarian SC, Jackman RW (2011) Identification of genes that elicit disuse muscle atrophy via the transcription factors p50 and Bcl-3. PLoS ONE 6(1):e16171. https://doi.org/10.1371/journal.pone.0016171

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Paul PK, Bhatnagar S, Mishra V, Srivastava S, Darnay BG, Choi Y, Kumar A (2012) The E3 ubiquitin ligase TRAF6 intercedes in starvation-induced skeletal muscle atrophy through multiple mechanisms. Mol Cell Biol 32(7):1248–1259. https://doi.org/10.1128/mcb.06351-11

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Vendrell J, Maymo-Masip E, Tinahones F, Garcia-Espana A, Megia A, Caubet E, Garcia-Fuentes E, Chacon MR (2010) Tumor necrosis-like weak inducer of apoptosis as a proinflammatory cytokine in human adipocyte cells: up-regulation in severe obesity is mediated by inflammation but not hypoxia. J Clin Endocrinol Metab 95(6):2983–2992. https://doi.org/10.1210/jc.2009-2481

    Article  CAS  PubMed  Google Scholar 

  32. Brown SA, Cheng E, Williams MS, Winkles JA (2013) TWEAK-independent Fn14 self-association and NF-kappaB activation is mediated by the C-terminal region of the Fn14 cytoplasmic domain. PLoS ONE 8(6):e65248. https://doi.org/10.1371/journal.pone.0065248

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Burkly LC, Dohi T (2011) The TWEAK/Fn14 Pathway in tissue remodeling: for better or for worse. In: Wallach D, Kovalenko A, Feldmann M (eds) Advances in TNF family research: proceedings of the 12th International TNF conference, 2009. Springer New York, New York, NY, pp 305–322. doi: 10.1007/978-1-4419-6612-4_32

  34. Pasiakos SM, Berryman CE, Carbone JW, Murphy NE, Carrigan CT, Bamman MM, Ferrando AA, Young AJ, Margolis LM (2018) Muscle Fn14 gene expression is associated with fat-free mass retention during energy deficit at high altitude. Physiol Rep 6(14):e13801. https://doi.org/10.14814/phy2.13801

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Bathgate KE, Bagley JR, Jo E, Talmadge RJ, Tobias IS, Brown LE, Coburn JW, Arevalo JA, Segal NL, Galpin AJ (2018) Muscle health and performance in monozygotic twins with 30 years of discordant exercise habits. Eur J Appl Physiol. https://doi.org/10.1007/s00421-018-3943-7

    Article  PubMed  Google Scholar 

  36. Raue U, Trappe TA, Estrem ST, Qian H-R, Helvering LM, Smith RC, Trappe S (2012) Transcriptome signature of resistance exercise adaptations: mixed muscle and fiber type specific profiles in young and old adults. J Appl Physiol 112(10):1625–1636. https://doi.org/10.1152/japplphysiol.00435.2011

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Raue U, Jemiolo B, Yang Y, Trappe S (2015) TWEAK-Fn14 pathway activation after exercise in human skeletal muscle: insights from two exercise modes and a time course investigation. J Appl Physiol 118(5):569–578. https://doi.org/10.1152/japplphysiol.00759.2014

    Article  CAS  PubMed  Google Scholar 

  38. Dogra C, Hall SL, Wedhas N, Linkhart TA, Kumar A (2007) Fibroblast growth factor inducible 14 (Fn14) is required for the expression of myogenic regulatory factors and differentiation of myoblasts into myotubes. Evidence for TWEAK-independent functions of Fn14 during myogenesis. J Biol Chem 282(20):15000–15010. https://doi.org/10.1074/jbc.M608668200

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  39. Burkly LC, Michaelson JS, Zheng TS (2011) TWEAK/Fn14 pathway: an immunological switch for shaping tissue responses. Immunol Rev 244(1):99–114. https://doi.org/10.1111/j.1600-065X.2011.01054.x

    Article  CAS  PubMed  Google Scholar 

  40. Darras BT, Miller DT, Urion DK (1993) Dystrophinopathies. In: Pagon RA, Adam MP, Ardinger HH et al. (eds) GeneReviews(R). University of Washington, Seattle, WA, USA. All rights reserved.

  41. Li H, Mittal A, Paul P, Kumar M, Srivastava D, Tyagi S, Kumar A (2009) Tumor necrosis factor-related weak inducer of apoptosis augments matrix metalloproteinase 9 (MMP-9) production in skeletal muscle through the activation of nuclear factor-kappa B-inducing kinase and p38 mitogen-activated protein kinase A potential role of MMP-9 in myopathy. J Biol Chem 284:4439–4450. https://doi.org/10.1074/jbc.M805546200

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Bakkar N, Guttridge DC (2010) NF-kappaB signaling: a tale of two pathways in skeletal myogenesis. Physiol Rev 90(2):495–511. https://doi.org/10.1152/physrev.00040.2009

    Article  CAS  PubMed  Google Scholar 

  43. Brown SAN, Ghosh A, Winkles JA (2010) Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-κB pathway. J Biol Chem 285(23):17432–17441. https://doi.org/10.1074/jbc.M110.131979

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Roos C, Wicovsky A, Muller N, Salzmann S, Rosenthal T, Kalthoff H, Trauzold A, Seher A, Henkler F, Kneitz C, Wajant H (2010) Soluble and transmembrane TNF-like weak inducer of apoptosis differentially activate the classical and noncanonical NF-kappa B pathway. J Immunol 185(3):1593–1605. https://doi.org/10.4049/jimmunol.0903555

    Article  CAS  PubMed  Google Scholar 

  45. Murphy RM, Lamb GD (2013) Important considerations for protein analyses using antibody based techniques: down-sizing western blotting up-sizes outcomes. J Physiol 591(Pt 23):5823–5831. https://doi.org/10.1113/jphysiol.2013.263251

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Murphy RM, Mollica JP, Beard NA, Knollmann BC, Lamb GD (2011) Quantification of calsequestrin 2 (CSQ2) in sheep cardiac muscle and Ca2+-binding protein changes in CSQ2 knockout mice. Am J Physiol Heart Circ Physiol 300(2):H595–604. https://doi.org/10.1152/ajpheart.00902.2010

    Article  CAS  PubMed  Google Scholar 

  47. Tong X, Yin L, Washington R, Rosenberg DW, Giardina C (2004) The p50–p50 NF-kappaB complex as a stimulus-specific repressor of gene activation. Mol Cell Biochem 265(1–2):171–183

    Article  CAS  Google Scholar 

  48. Bakkar N, Wang J, Ladner KJ, Wang H, Dahlman JM, Carathers M, Acharyya S, Rudnicki MA, Hollenbach AD, Guttridge DC (2008) IKK/NF-kappaB regulates skeletal myogenesis via a signaling switch to inhibit differentiation and promote mitochondrial biogenesis. J Cell Biol 180(4):787–802. https://doi.org/10.1083/jcb.200707179

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  49. Alvarez-Guardia D, Palomer X, Coll T, Davidson MM, Chan TO, Feldman AM, Laguna JC, Vazquez-Carrera M (2010) The p65 subunit of NF-kappaB binds to PGC-1alpha, linking inflammation and metabolic disturbances in cardiac cells. Cardiovasc Res 87(3):449–458. https://doi.org/10.1093/cvr/cvq080

    Article  CAS  PubMed  Google Scholar 

  50. Sato S, Ogura Y, Kumar A (2014) TWEAK/Fn14 signaling axis mediates skeletal muscle atrophy and metabolic dysfunction. Front Immunol 5:18. https://doi.org/10.3389/fimmu.2014.00018

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  51. Dogra C, Changotra H, Mohan S, Kumar A (2006) Tumor necrosis factor-like weak inducer of apoptosis inhibits skeletal myogenesis through sustained activation of nuclear factor-kappaB and degradation of MyoD protein. J Biol Chem 281(15):10327–10336. https://doi.org/10.1074/jbc.M511131200

    Article  CAS  PubMed  Google Scholar 

  52. Enwere EK, Holbrook J, Lejmi-Mrad R, Vineham J, Timusk K, Sivaraj B, Isaac M, Uehling D, Al-awar R, LaCasse E, Korneluk RG (2012) TWEAK and cIAP1 regulate myoblast fusion through the noncanonical NF-kappaB signaling pathway. Sci Signal 5(246):ra75. https://doi.org/10.1126/scisignal.2003086

    Article  CAS  PubMed  Google Scholar 

  53. Varfolomeev E, Goncharov T, Maecker H, Zobel K, Komuves LG, Deshayes K, Vucic D (2012) Cellular inhibitors of apoptosis are global regulators of NF-kappaB and MAPK activation by members of the TNF family of receptors. Sci Signal 5(216):ra22. https://doi.org/10.1126/scisignal.2001878

    Article  CAS  PubMed  Google Scholar 

  54. Hu WH, Johnson H, Shu HB (2000) Activation of NF-kappaB by FADD, Casper, and caspase-8. J Biol Chem 275(15):10838–10844

    Article  CAS  Google Scholar 

  55. Ikner A, Ashkenazi A (2011) TWEAK induces apoptosis through a death-signaling complex comprising receptor-interacting protein 1 (RIP1), Fas-associated death domain (FADD), and caspase-8. J Biol Chem 286(24):21546–21554. https://doi.org/10.1074/jbc.M110.203745

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  56. Cargnello M, Roux PP (2011) Activation and function of the MAPKs and their substrates, the MAPK-activated protein kinases. Microbiol Mol Biol Rev 75(1):50–83. https://doi.org/10.1128/mmbr.00031-10

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  57. Jones NC, Fedorov YV, Rosenthal RS, Olwin BB (2001) ERK1/2 is required for myoblast proliferation but is dispensable for muscle gene expression and cell fusion. J Cell Physiol 186(1):104–115. https://doi.org/10.1002/1097-4652(200101)186:1%3c104:aid-jcp1015%3e3.0.co;2-0

    Article  CAS  PubMed  Google Scholar 

  58. Coolican SA, Samuel DS, Ewton DZ, McWade FJ, Florini JR (1997) The mitogenic and myogenic actions of insulin-like growth factors utilize distinct signaling pathways. J Biol Chem 272(10):6653–6662

    Article  CAS  Google Scholar 

  59. Xie S-J, Li J-H, Chen H-F, Tan Y-Y, Liu S-R, Zhang Y, Xu H, Yang J-H, Liu S, Zheng L-L, Huang M-B, Guo Y-H, Zhang Q, Zhou H, Qu L-H (2018) Inhibition of the JNK/MAPK signaling pathway by myogenesis-associated miRNAs is required for skeletal muscle development. Cell Death Differ 25(9):1581–1597. https://doi.org/10.1038/s41418-018-0063-1

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  60. Keren A, Tamir Y, Bengal E (2006) The p38 MAPK signaling pathway: a major regulator of skeletal muscle development. Mol Cell Endocrinol 252(1–2):224–230. https://doi.org/10.1016/j.mce.2006.03.017

    Article  CAS  PubMed  Google Scholar 

  61. Cabane C, Englaro W, Yeow K, Ragno M, Derijard B (2003) Regulation of C2C12 myogenic terminal differentiation by MKK3/p38alpha pathway. Am J Physiol Cell Physiol 284(3):C658–666. https://doi.org/10.1152/ajpcell.00078.2002

    Article  CAS  PubMed  Google Scholar 

  62. Jin B, Li YP (2007) Curcumin prevents lipopolysaccharide-induced atrogin-1/MAFbx upregulation and muscle mass loss. J Cell Biochem 100(4):960–969. https://doi.org/10.1002/jcb.21060

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Bodine SC, Stitt TN, Gonzalez M, Kline WO, Stover GL, Bauerlein R, Zlotchenko E, Scrimgeour A, Lawrence JC, Glass DJ, Yancopoulos GD (2001) Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nat Cell Biol 3(11):1014–1019. https://doi.org/10.1038/ncb1101-1014

    Article  CAS  PubMed  Google Scholar 

  64. Stitt TN, Drujan D, Clarke BA, Panaro F, Timofeyva Y, Kline WO, Gonzalez M, Yancopoulos GD, Glass DJ (2004) The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors. Mol Cell 14(3):395–403. https://doi.org/10.1016/s1097-2765(04)00211-4

    Article  CAS  PubMed  Google Scholar 

  65. Wajant H (2013) The TWEAK-Fn14 system as a potential drug target. Br J Pharmacol 170(4):748–764. https://doi.org/10.1111/bph.12337

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  66. Sanz AB, Sanchez-Niño MD, Carrasco S, Manzarbeitia F, Ruiz-Andres O, Selgas R, Ruiz-Ortega M, Gonzalez-Enguita C, Egido J, Ortiz A (2012) Inflammatory cytokines and survival factors from serum modulate tweak-induced apoptosis in PC-3 prostate cancer cells. PLoS ONE 7(10):e47440–e47440. https://doi.org/10.1371/journal.pone.0047440

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  67. Fortin SP, Ennis MJ, Savitch BA, Carpentieri D, McDonough WS, Winkles JA, Loftus JC, Kingsley C, Hostetter G, Tran NL (2009) Tumor necrosis factor-like weak inducer of apoptosis stimulation of glioma cell survival is dependent on Akt2 function. Mol Cancer Res 7(11):1871–1881. https://doi.org/10.1158/1541-7786.mcr-09-0194

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  68. Ando T, Ichikawa J, Wako M, Hatsushika K, Watanabe Y, Sakuma M, Tasaka K, Ogawa H, Hamada Y, Yagita H, Nakao A (2006) TWEAK/Fn14 interaction regulates RANTES production, BMP-2-induced differentiation, and RANKL expression in mouse osteoblastic MC3T3-E1 cells. Arthritis Res Ther 8(5):R146. https://doi.org/10.1186/ar2038

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  69. Yang B, Yan P, Gong H, Zuo L, Shi Y, Guo J, Guo R, Xie J, Li B (2016) TWEAK protects cardiomyocyte against apoptosis in a PI3K/AKT pathway dependent manner. Am J Transl Res 8(9):3848–3860

    CAS  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

This research was supported by an Australian Government Research Training Program (RTP) Scholarship to ALP. Figures created with BioRender.com.

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  1. Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, 3086, Australia

    Amy L. Pascoe, Amelia J. Johnston & Robyn M. Murphy

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Pascoe, A.L., Johnston, A.J. & Murphy, R.M. Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration. Cell. Mol. Life Sci. 77, 3369–3381 (2020). https://doi.org/10.1007/s00018-020-03495-x

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