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Diagnostic and therapeutic potential of transforming growth factor beta 1 in solid organ transplantation: recent research findings ; Диагностический и терапевтический потенциал трансформирующего фактора роста β1 при трансплантации солидных органов: результаты последних исследований

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  • معلومة اضافية
    • بيانات النشر:
      Academician V.I.Shumakov National Medical Research Center of Transplantology and Artificial Organs", Ministry of Health of the Russian Federation
    • الموضوع:
      2023
    • Collection:
      Russian Journal of Transplantology and Artificial Organs / Вестник трансплантологии и искусственных органов
    • نبذة مختصرة :
      Federation Clinical outcomes of solid organ transplantation depend on many factors. One of the main factors is the risk of post-transplant complications, which affect allograft and recipient survival. Multifactorial organ damage in post-transplant complications and the search for diagnostic and prognostic indicators of the condition have contributed to the study and selection of a wide range of proteomic and molecular genetic biomarkers, which have shown to be effective in solid organ transplantation. The use of biomarkers opens up additional possibilities for assessing the risk of complications and their early diagnosis. This potentially reduces the frequency of invasive diagnostic procedures. Transforming growth factor beta 1 (TGF-β1) regulates many biological processes, has anti-inflammatory and immunosuppressive effects, participates in immune response, and plays a key role in extracellular matrix (ECM) protein synthesis. ECM dysregulation leads to fibroblast hyperproliferation and increased collagen synthesis and, consequently, tissue fibrosis. The variability of the diagnostic and prognostic potential of TGF-β1 has been demonstrated in studies on recipients of various solid organs. The objective of this review is to analyze recent evidence on the role of TGF-β1 in the development of post-transplant complications and to assess its prospects as a marker of graft pathology or as a target for therapy. ; Клинические результаты трансплантации солидных органов зависят от многих факторов, и главным среди них остается риск развития посттрансплантационных осложнений, ограничивающих выживаемость аллотрансплантата и реципиента. Концепция многофакторности повреждения органа при развитии посттрансплантационных осложнений и поиск диагностических и прогностических индикаторов патологии способствовали изучению и отбору широкого спектра протеомных и молекулярно-генетических биомаркеров, показавших эффективность при трансплантации солидных органов. Применение биомаркеров открывает дополнительные возможности для оценки риска ...
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      application/pdf
    • Relation:
      https://journal.transpl.ru/vtio/article/view/1645/1479; Choi J, Bano A, Azzi J. Biomarkers in Solid Organ Transplantation. Clin Lab Med. 2019; 39 (1): 73–85.; Tzavlaki K, Moustakas A. TGF-β Signaling. Biomolecules. 2020; 10 (3): 487.; Zhang H, Yang P, Zhou H, Meng Q, Huang X. Involvement of Foxp3-expressing CD4+ CD25+ regulatory T cells in the development of tolerance induced by transforming growth factor-beta2-treated antigen-presenting cells. Immunology. 2008; 124: 304–314.; Javelaud D, Mauviel A. Mammalian transforming growth factor-βs: smad signaling and physio-pathological roles. International Journal of Biochemistry and Cell Biology. 2004; 36 (7): 1161–1165.; Poniatowski LA, Wojdasiewicz P, Gasik R, Szukiewicz D. Transforming growth factor beta family: insight into the role of growth factors in regulation of fracture healing biology and potential clinical applications. Mediators Inflamm. 2015; 2015: 137823.; Wilson SE. TGF beta-1, -2 and -3 in the modulation of fibrosis in the cornea and other organs. Exp Eye Res. 2021; 207: 108594.; Verrecchia F, Mauviel A. Transforming growth factor-β signaling through the smad pathway: role in extracellular matrix gene expression and regulation. J Invest Dermatol. 2002; 118 (2): 211–215.; Wang W, Huang XR, Canlas E, Oka K, Truong LD, Deng C et al. Essential role of Smad3 in angiotensin IIinduced vascular fibrosis. Circ Res. 2006; 98 (8): 1032– 1039.; Vander Ark A, Cao J, Li X. TGF-β receptors: in and beyond TGF-β signaling. Cell Signal. 2018; 52: 112–120.; Chen L, Yang T, Lu DW, Zhao H, Feng YL, Chen H et al. Central role of dysregulation of TGF-β/Smad in CKD progression and potential targets of its treatment. Biomed Pharmacother. 2018; 101: 670–681.; Fujimoto M, Maezawa Y, Yokote K, Joh K, Kobayashi K, Kawamura H et al. Mice lacking Smad3 are protected against streptozotocin-induced diabetic glomerulopathy. Biochem Biophys Res Commun. 2003; 305: 1002–1007.; Shah R, Tanriverdi K, Levy D, Larson M, Gerstein M, Mick E et al. Discordant expression of circulating microRNA from cellular and extracellular sources. PLoS One. 2016; 11 (4): e0153691.; Novák J, Macháčková T, Krejčí J, Bienertová­Vašků J, Slabý O. MicroRNAs as theranostic markers in cardiac allograft transplantation: from murine models to clinical practice. Theranostics. 2021; 11 (12): 6058–6073.; Gu YY, Dou JY, Huang XR, Liu XS, Lan HY. Transforming growth factor-β and long non-coding rna in renal inflammation and fibrosis. Front Physiol. 2021; 12: 684236.; Zhang XL, An BF, Zhang GC. MiR-27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF-κB pathway. Kaohsiung J Med Sci. 2019; 35 (10): 607–614.; Suzuki HI, Katsura A, Mihira H, Horie M, Saito A, Miyazono K. Regulation of TGF-β-mediated endothelialmesenchymal transition by microRNA-27. J Biochem. 2017; 161 (5): 417–420.; Wang XH. MicroRNA in myogenesis and muscle atrophy. Curr Opin Clin Nutr Metab Care. 2013; 16 (3): 258–266.; Dong M, Wang X, L T, Wang J, Yang Y, Liu Y et al. Mir27a-3p attenuates bronchiolitis obliterans in vivo via the regulation of dendritic cells’ maturation and the suppression of myofibroblasts’ differentiation. Clin Transl Med. 2020; 10 (4): e140.; Шевченко ОП, Великий ДА, Шарапченко СО, Гичкун ОЕ, Марченко АВ, Улыбышева АА и др. МикроРНК-27 и -339 при фиброзе миокарда трансплантированного сердца: анализ диагностической значимости. Вестник трансплантологии и искусственных органов. 2021; 23 (3): 73–81.; Великий ДА, Гичкун ОЕ, Шарапченко СО, Можейко НП, Курабекова РМ, Шевченко ОП и др. Диагностическое значение микроРНК-101 и микроРНК-27 при остром отторжении трансплантированного сердца. Вестник трансплантологии и искусственных органов. 2020; 22 (4): 20–26.; Cuiqiong W, Chao X, Xinling F, Yinyan J. Schisandrin B suppresses liver fibrosis in rats by targeting miR-101-5p through the TGF-β signaling pathway. Artif Cells Nanomed Biotechnol. 2020; 48 (1): 473–478.; Li X, Zhang S, Wa M, Liu Z, Hu S. MicroRNA-101 protects against cardiac remodeling following myocardial infarction via downregulation of runt-related transcription factor 1. J Am Heart Assoc. 2019; 8 (23): e013112.; Pan Z, Sun X, Shan H, Wang N, Wang J, Ren J et al. MicroRNA-101 inhibited postinfarct cardiac fibrosis and improved left ventricular compliance via the FBJ osteosarcoma oncogene/transforming growth factor-β1 pathway. Circulation. 2012; 126 (7): 840–850.; Guiot J, Cambier M, Boeckx A, Henket M, Nivelles O, Gester F et al. Macrophage-derived exosomes attenuate fibrosis in airway epithelial cells through delivery of antifibrotic miR-142-3p. Thorax. 2020; 75 (10): 870–881.; Jung B, Staudacher JJ, Beauchamp D. Transforming growth factor β super-family signaling in development of colorectal cancer. Gastroenterology. 2017; 152: 36–52.; Meng XM, Nikolic­Paterson DJ, Lan HY. TGF-β: the master regulator of fibrosis. Nat Rev Nephrol. 2016; 12 (6): 325–338.; Okamoto Y, Gotoh Y, U emura O, Tanaka S, Ando T, Nishida M. Age-dependent decrease in serum transforming growth factor TGF-beta 1 in healthy Japanese individuals; population study of serum TGF-beta 1 level in Japanese. Dis Markers. 2005; 21 (2): 71–74.; Курабекова РМ, Шевченко ОП, Цирульникова ОМ, Можейко НП, Цирульникова ИЕ, Олефиренко ГА. Связь уровня трансформирующего фактора роста бета 1 с фиброзом печени у детей с врожденными заболеваниями гепатобилиарной системы. Клиническая лабораторная диагностика. 2017; 62 (4): 221– 225.; Travis MA, Sheppard D. TGF-b Activation and Function in Immunity. Annu Rev Immunol. 2014; 32 (1): 51–82.; Курабекова РМ, Шевченко ОП, Цирульникова ОМ, Можейко НП, Цирульникова ИЕ, Монахов АР, Готье СВ. Уровень трансформирующего фактора роста бета-1 связан с тяжестью врожденных заболеваний печени у детей раннего возраста. Вестник трансплантологии и искусственных органов. 2016; 18 (3): 16–21.; Briem­Richter A, Leuschner A, Krieger T, Grabhorn E, Fischer L, Nashan B et al. Peripheral blood biomarkers for the characterization of alloimmune reactivity after pediatric liver transplantation. Pediatr Transplant. 2013; 17 (8): 757–764.; Israni AK, Li N, Cizman BB, Snyder J, Abrams J, Joffe M et al. Association of donor inflammation- and apoptosis-related genotypes and delayed allograft function after kidney transplantation. Am J Kidney Dis. 2008; 52: 331–339.; Lee SB, Kanasaki K, Kalluri R. Circulating TGF-Β1 as a reliable biomarker for chronic kidney disease progression in the African-American population. Kidney Int. 2009; 76: 10–12.; Meng XM, Nikolic­Paterson DJ, Lan HY. Inflammatory processes in renal fibrosis. Nat Rev Nephrol. 2014; 10: 493–503.; Yuan Q, Tan RJ, Liu Y. Myofibroblast in kidney fibrosis: origin, activation, and regulation. Adv Exp Med Biol. 2019; 1165: 253–283.; Shull MM, Ormsby I, Kier AB, Pawlowski S, Diebold RJ, Yin M et al. Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease. Nature. 1992; 359: 693–699.; Eikmans M, Sijpkens YW, Baelde HJ, de Heer E, Paul LC, Bruijn JA. High transforming growth factor-β and extracellular matrix mRNA response in renal allografts during early acute rejection is associated with absence of chronic rejection. Transplantation. 2002; 73: 573–579.; Du XX, Guo YL, Yang M, Yu Y, Chang S, Liu B et al. Relationship of transforming growth factor-βl and arginase-1 levels with long-term survival after kidney transplantation. Curr Med Sci. 2018; 38: 455–460.; Poppelaars F, Gaya da Costa M, Faria B, Eskandari SK, Damman J, Seelen MA. A functional TGFB1 polymorphism in the donor associates with long-term graft survival after kidney transplantation. Clin Kidney J. 2021; 15 (2): 278–286.; Sun Y, Weber KT. Infarct scar: a dynamic tissue. Cardiovasc Res. 2000; 46 (2): 250–256.; Moses HL. TGF-beta regulations of epithelial cell proliferation. Mol Prod Dev. 1992; 32 (2): 179–183.; Гичкун ОЕ, Курабекова РМ, Олефиренко ГА, Стаханова ЕА, Макарова ЛВ, Шмерко НП и др. Динамика трансформирующего фактора роста бета-1 у реципиентов сердца. Вестник трансплантологии и искусственных органов. 2019; 21: 56.; Karch DB, Billingham ME. Cyclosporin-induced myocardial fibrosis: An unequally controlled case report. Heart Transplant. 1985; 4: 210–212.; Frangogiannis NG. Cardiac fibrosis. Cardiovasc Res. 2021; 117 (6): 1450–1488.; Aziz T, Saad RA, Burgess M, Yonan N, Hasleton P, Hutchinson IV. Transforming growth factor beta and myocardial dysfunction following heart transplantation. European Journal of Cardio­Thoracic Surgery. 2001; 20 (1): 177–186.; Aziz T, Saad RA, Burgess M, Yonan N, Hasleton P, Hutchinson IV. Transforming growth factor β in relation to cardiac allograft vasculopathy after heart transplantation. J Thorac Cardiovasc Surg. 2000; 119: 700–708.; Гичкун ОЕ, Шевченко ОП, Курабекова РМ, Можейко НП, Шевченко АО. Полиморфизм rs1800470 гена tgfb1 связан с фиброзом миокарда у реципиентов сердца. Acta Naturae (русскоязычная версия). 2021; 13 (4): 42–46.; DerHovanessian A, Weigt SS, Palchevskiy V, Shino MY, Sayah DM, Gregson AL et al. The role of TGF-β in the association between primary graft dysfunction and bronchiolitis obliterans syndrome. Am J Transplant. 2016; 16 (2): 640–649.; Stewart S, Fishbein MC, Snell GI, Berry GJ, Boehler A, Burke MM et al. Revision of the 1996 working formulation for the standardization of nomenclature in the diagnosis of lung rejection. J Heart Lung Transplant. 2007; 26: 1229–1242.; Westall GP, Snel GI, Loskot M, Levvey B, O’Hehir RE, Hedger MP, de Kretser DM. Activin biology after lung transplantation. Transplant Direct. 2017; 3 (6): e159.; Sime PJ, Xing Z, Graham FL, Csaky KG, Gauldie J. Adenovector-mediated gene transfer of active transforming growth factor-beta1 induces prolonged severe fibrosis in rat lung. J Clin Invest. 1997; 100: 768–776.; Charpin JM, Valcke J, Kettaneh L, Epardeau B, Stern M, Israël­Biet D. Peaks of transforming growth factor-β in alveolar cells of lung transplant recipients as an early marker of chronic rejection. Transplantation. 1998; 65 (5): 752–755.; Yue YL, Zhang MY, Liu JY, Fang LJ, Qu YQ. The role of autophagy in idiopathic pulmonary fibrosis: from mechanisms to therapies. Ther Adv RespirDis. 2022; 16: 17534666221140972.; Ye Z, Hu Y. TGF-β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review). Int J Mol Med. 2021; 48 (1): 132.; Cohen DJ, Loertcher R, Rubin MF, Tilney NL, Carpenter CB, Strom TB. Cyclosporine: A New Immunosuppressive Agent for Organ Transplantation. Ann Intern Med. 1984; 101: 667–682.; Bentata Y. Tacrolimus: 20 years of use in adult kidney transplantation. What we should know about its nephrotoxicity. Artif Organs. 2020; 44 (2): 140–152.; Liu Q, Ye J, Yu L, Dong X, Feng J, Xiong Y et al. Mitigates Cyclosporine A (CsA)-Induced Epithelial-Mesenchymal Transition (EMT) and Renal Fibrosis in Rats. Int Urol Nephrol. 2017; 49: 345–352.; Nagavally RR, Sunilkumar S, Akhtar M, Trombetta LD, Ford SM. Chrysin Ameliorates Cyclosporine-A-Induced Renal Fibrosis by Inhibiting TGF-β1-Induced EpithelialMesenchymal Transition. Int J Mol Sci. 2021; 22 (19): 10252.; Khanna A, Plummer M, Bromberek C, Bresnahan B, Hariharan S. Expression of TGF-beta and fibrogenic genes in transplant recipients with tacrolimus and cyclosporine nephrotoxicity. Kidney Int. 2002; 62: 2257–2263.; Zhang LY, Jin J, Luo K, Piao SG, Zheng HL, Jin JZ et al. Shen-Kang protects against tacrolimus-induced renal injury. Korean J Intern Med. 2019; 34 (5): 1078–1090.; Boix F, Alfaro R, Jiménez­Coll V, Mrowiec A, MartínezBanaclocha H, Botella C, Muro M. A high concentration of TGF-β correlates with opportunistic infection in liver and kidney transplantation. Human Immunology. 2021; 82 (6): 414–421.; Neuzillet C, Tijeras­Raballand A, Cohen R, Cros J, Faivre S, Raymond E, de Gramont A. Targeting the TGFβ pathway for cancer therapy. Pharmacol Ther. 2015; 147: 22–31.; Border WA, Okuda S, Languino LR, Sporn MB, Ruoslahti E. Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1. Nature. 1990; 346: 371–374.; Kasuga H, Ito Y, Sakamoto S, Kawachi H, Shimizu F, Yuzawa Y, Matsuo S. Effects of anti-TGF-β type II receptor antibody on experimental glomerulonephritis. Kidney Int. 2001; 60: 1745–1755.; Das S, Kumar M, Negi V, Pattnaik B, Prakash YS, Agrawal A, Ghosh B. MicroRNA-326 regulates profibrotic functions of transforming growth factor-β in pulmonary fibrosis. Am J Respir Cell Mol Biol. 2014; 50 (5): 882– 892.; Isaka Y. Targeting TGF-β Signaling in Kidney Fibrosis. Int J Mol Sci. 2018; 19 (9): 2532.; De Streel G, Bertrand C, Chalon N, Liénart S, Bricard O, Lecomte S et al. Selective inhibition of TGF-β1 produced by GARP-expressing Tregs overcomes resistance to PD-1/PD-L1 blockade in cancer. Nat Commun. 2020; 11 (1): 4545.; Nakano T, Lai CY, Goto S, Hsu LW, Kawamoto S, Ono K et al. Immunological and regenerative aspects of hepatic mast cells in liver allograft rejection and tolerance. PloS One. 2012; 7 (5): 15.; Luangmonkong T, Suriguga S, Bigaeva E, Boersema M, Oosterhuis D, de Jong KP et al. Evaluating the antifibrotic potency of galunisertib in a human ex vivo model of liver fibrosis. Br J Pharmacol. 2017; 174: 3107–3117.; https://journal.transpl.ru/vtio/article/view/1645
    • الرقم المعرف:
      10.15825/1995-1191-2023-2-148-157
    • Rights:
      Authors who publish with this journal agree to the following terms:Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access). ; Авторы, публикующие в данном журнале, соглашаются со следующим:Авторы сохраняют за собой авторские права на работу и предоставляют журналу право первой публикации работы на условиях лицензии Creative Commons Attribution License, которая позволяет другим распространять данную работу с обязательным сохранением ссылок на авторов оригинальной работы и оригинальную публикацию в этом журнале.Авторы сохраняют право заключать отдельные контрактные договорённости, касающиеся не-эксклюзивного распространения версии работы в опубликованном здесь виде (например, размещение ее в институтском хранилище, публикацию в книге), со ссылкой на ее оригинальную публикацию в этом журнале.Авторы имеют право размещать их работу в сети Интернет (например в институтском хранилище или персональном сайте) до и во время процесса рассмотрения ее данным журналом, так как это может привести к продуктивному обсуждению и большему количеству ссылок на данную работу (См. The Effect of Open Access).
    • الرقم المعرف:
      edsbas.52E12E8C