Development of liver fibrosis. Present and future possibilities of correction in children

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Abstract

Liver fibrosis (LF) is a natural consequence of almost all liver diseases of any etiology. Considering the pathogenesis of AF, we are faced with a number of standard stereotypical processes that unfold in the liver tissue. These are mainly processes of chronic inflammation, which are opposed by the processes of regeneration of liver tissues. The basis of the imbalance between the processes of fibrosis and regeneration is the accumulation of the extracellular matrix. Liver fibrosis in its development leads to cirrhosis of the liver, hepatocellular carcinoma, and an increase in the incidence is observed throughout the world. Although this is a genetically determined process, modifiable factors play an important role in the progression of this disease. Current evidence suggests the possibility of reversible liver fibrosis. Understanding the molecular mechanisms of AF development is a key area of work for scientists involved in the development of antifibrotic therapy. The article discusses modern views on the treatment/prevention of the disease and the prospects for influencing the processes of liver fibrosis with an emphasis on childhood.

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About the authors

Konstantin Ivanovich Grigoryev

Russian National Research Medical University. N.I. Pirogov of the Ministry of Health of Russia

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Email: k-i-grigoryev@yandex.ru
Doctor of Medical Sciences, Professor of the Department of Pediatrics with Infectious Diseases in Children, FDPO

References

  1. Кулебина E.A., Сурков A.H. Механизмы формирования фиброза печени: современные представления. Педиатрия. 2019; 98 (6): 166-170. doi.org/10.24110/0031-403X-2019-98-6-166-170.
  2. Сурков А.Н., Смирнов И.Е., Кучеренко и др. Взаимосвязи сывороточных маркеров фиброзирования с изменениями структурно-функционального состояния печени у детей. Российский педиатрический журнал. 2010; 2: 28-31.
  3. Цуканов В. В., Юркина А. С., Ушакова Т. А. и др. Эпидемиологические особенности неалкогольной жировой болезни печени в Новосибирске (Сибирский федеральный округ): региональные данные открытого многоцентрового проспективного исследования DIREG 2. Современная фармакоэкономика и фармакоэпидемиология. 2016; 2: 17-27.
  4. Потешкина Н.Г., Аджигайтканова С.К. Современные принципы диагностики и лечения осложнений цирроза печени: учебно-методическое пособие. - М., РНИМУ им. Н.И.Пирогова, 2013; 44 с.
  5. Iwaisako K., Jiang C., Zhang M., et al. Origin of myofibroblasts in the fibrotic liver in mice. Proc. Natl. Acad. Sci. USA. 2014; 111 (32): 3297-3305. doi: 10.1073/pnas.1400062111.
  6. Hinz B. Myofibroblasts. Exp. Eye Res. 2016; 142: 56-70. doi: 10.1016/j.exer.2015.07.009
  7. Gabbiani G. 50 Years of Myofibroblasts: How the Myofibroblast Concept Evolved. Methods Mol Biol. 2021; 2299: 1-5. doi: 10.1007/978-1-0716-1382-5_1
  8. Seki E., Brenner D. Recent advancement of molecular mechanisms of liver fibrosis. J. Hepatobiliary Pancreat. Sci. 2015; 22 (7): 512-518. doi: 10.1002/jhbp.245.
  9. Tacke F., Trautwein C. Mechanisms of liver fibrosis resolution. J. Hepatol. 2015; 63 (4): 1038-9. doi: 10.1016/j.jhep.2015.03.039
  10. Bi WR, Yang CO, Shi O. Transforming growth factor-pi induced epithelial-mesenchymal transition in hepatic fibrosis. Hepatogastroenterology. 2012; 59(118):1960-3. doi: 10.5754/hge11750.
  11. Taura K., Miura K., Iwaisako K., et al. Hepatocytes do not undergo epithelial-mesenchymal transition in liver fibrosis in mice. Hepatology. 2010; 51 (3): 1027-1036. doi: 10.1002/hep.23368
  12. Chu AS, Diaz R., Hui JJ, et al. Lineage tracing demonstrates no evidence of cholangiocyte epithelial-to-mesenchymal transition in murine models of hepatic fibrosis. Hepatology. 2011; 53 (5): 16851695. doi: 10.1002/hep.24206
  13. Lua I., James D., Wang J., et al. Mesodermal mesenchymal cells give rise to myofibroblasts, but not epithelial cells, in mouse liver injury. Hepatology. 2014; 60 (1): 311-22. doi: 10.1002/hep.27035
  14. Zhang W., Conway SJ, Liu Y., et al. Heterogeneity of Hepatic Stellate Cells in Fibrogenesis of the Liver: Insights from Single-Cell Transcriptomic Analysis in Liver Injury. Cells. 2021 Aug 19;10 (8): 21-29. doi: 10.3390/cells10082129.
  15. Харитонова Л.А., Григорьев К.И., Запруднов A.M. От идеи к реалиям: современные успехи детской гастроэнтерологии. Экспериментальная и клиническая гастроэнтерология. 2019; 171 (11): 4-15. doi: 10.31146/1682-8658-ecg-171-11-4-15
  16. Ивлева С.А., Дворяковская Г.М., Четкина Т.С., и др. Диагностика фиброза печени у детей с болезнью Вильсона. Российский педиатрический журнал. 2014: 3: 9-14.
  17. Ивашкин В.Т., Маевская М.В., Павлов Ч.С., и др. Клинические рекомендации по диагностике и лечению неалкогольной жировой болезни печени Российского общества по изучению печени и Российской гастроэнтерологической ассоциации. Российский журнал гастроэнтерологии, гепатологии, колопроктологии. 2016; 26 (2): 24-42. https://doi.org/10.22416/1382-4376-2016-26-2-24-42
  18. Дуда А.К., Окружное Н.В., Бойко В.А., и др. Фиброз печени: современные принципы диагностики. Актуальная инфектология. 2014; 3 (4): 59-65.
  19. Gundermann, K.-J., Gundermann S., Drozdzik M., et al. Essential phospholipids in fatty liver: a scientific update. Clinical and experimental gastroenterology. 2016; 9:105-17. doi: 10.2147/CEG.S96362
  20. Tang PC, Zhang YY, Li JS, et al. LncRNA-Dependent Mechanisms of Transforming Growth Factor-β: From Tissue Fibrosis to Cancer Progression. Noncoding RNA. 2022; 8 (3): 36p. doi: 10.3390/ncrna8030036.
  21. Kanmani P, Kim H. Probiotics counteract the expression of hepatic profibrotic genes via the attenuation of TGF-β/SMAD signaling and autophagy in hepatic stellate cells. PLoS One, 2022; 17. :e0262767. doi: 10.1371/journal.pone.0262767
  22. Ohashi T., Yamamoto T. Antifibrotic effect of lysophosphatidic acid receptors LPA1 and LPA3 antagonist on experimental murine scleroderma induced by bleomycin. Exp. Dermatol. 2015; 24: 698702. doi: 10.1111/exd.12752.
  23. Lu O., Zhou Y., Xu M., et al. Sequential delivery for hepatic fibrosis treatment based on carvedilol loaded star-like nanozyme. J. Control Release 2021; 341: 247-60. doi: 10.1016/j. jconrel.2021.11.033
  24. Евсеенко Д.А., Дундаров 3.A., Надыров Э.А., Майоров В.М. Комплексная оценка эффективности антиоксидантной терапии у пациентов с острым кровотечением на фоне цирроза печени. Гепатология и гастроэнтерология. 2020; 4 (1): 68-75. https://doi.org/10.25298/2616-5546-2020-4-1-68-75
  25. Xu F., Tautenhahn HM, Dirsch O., et al. Modulation of Autophagy: A Novel «Rejuvenation» Strategy for the Aging Liver. Oxid Med Cell Longev 2021; 2021:6611126. doi: 10.1155/2021/6611126
  26. Lin X., Han L., Weng J., et al. Rapamycin inhibits proliferation and induces autophagy in human neuroblastoma cells. Bioscience Reports. 2018;38(6, article BSR20181822) doi: 10.1042/BSR20181822
  27. Pinto R.B., Schneider A.C.R., da Silveira Th.R. Cirrhosis in children and adolescents: An overview. World J. Hepatol. 2015; 7(3): 392-405. doi: 10.4254/wjh.v7.i3.392

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