본문 바로가기
KERD
논문KCI 등재

Cellular and Molecular Mechanisms of Intestinal Fibrosis

1

조회

0

다운로드

0

인용

0

참고문헌

키워드

초록

Intestinal fibrosis associated stricture is a common complication of inflammatory bowel disease usually requiring endoscopic or surgical intervention. Effective anti-fibrotic agents aiming to control or reverse intestinal fibrosis are still unavailable. Thus, clarifying the mechanism underpinning intestinal fibrosis is imperative. Fibrosis is characterized by an excessive accumulation of extracellular matrix (ECM) proteins at the injured sites. Multiple cellular types are implicated in fibrosis development. Among these cells, mesenchymal cells are major compartments that are activated and then enhance the production of ECM. Additionally, immune cells contribute to the persistent activation of mesenchymal cells and perpetuation of inflammation. Molecules are messengers of crosstalk between these cellular compartments. Although inflammation is necessary for fibrosis development, purely controlling intestinal inflammation cannot halt the development of fibrosis, suggesting that chronic inflammation is not the unique contributor to fibrogenesis. Several inflammation-independent mechanisms including gut microbiota, creeping fat, ECM interaction, and metabolic reprogramming are involved in the pathogenesis of fibrosis. In the past decades, substantial progress has been made in elucidating the cellular and molecular mechanisms of intestinal fibrosis. Here, we summarized new discoveries and advances of cellular components and major molecular mediators that are associated with intestinal fibrosis, aiming to provide a basis for exploring effective anti-fibrotic therapies in this field.

Abstract

Intestinal fibrosis associated stricture is a common complication of inflammatory bowel disease usually requiring endoscopic or surgical intervention. Effective anti-fibrotic agents aiming to control or reverse intestinal fibrosis are still unavailable. Thus, clarifying the mechanism underpinning intestinal fibrosis is imperative. Fibrosis is characterized by an excessive accumulation of extracellular matrix (ECM) proteins at the injured sites. Multiple cellular types are implicated in fibrosis development. Among these cells, mesenchymal cells are major compartments that are activated and then enhance the production of ECM. Additionally, immune cells contribute to the persistent activation of mesenchymal cells and perpetuation of inflammation. Molecules are messengers of crosstalk between these cellular compartments. Although inflammation is necessary for fibrosis development, purely controlling intestinal inflammation cannot halt the development of fibrosis, suggesting that chronic inflammation is not the unique contributor to fibrogenesis. Several inflammation-independent mechanisms including gut microbiota, creeping fat, ECM interaction, and metabolic reprogramming are involved in the pathogenesis of fibrosis. In the past decades, substantial progress has been made in elucidating the cellular and molecular mechanisms of intestinal fibrosis. Here, we summarized new discoveries and advances of cellular components and major molecular mediators that are associated with intestinal fibrosis, aiming to provide a basis for exploring effective anti-fibrotic therapies in this field.

참고문헌 (198)

  1. Wynn TA, "Mechanisms of fibrosis : therapeutic translation for fibrotic disease", Nat Med, 18, pp.1028~1040 (2012)
  2. Henderson NC, "Fibrosis : from mechanisms to medicines", Nature, 587, pp.555~566 (2020)
  3. Weiskirchen R, "Organ and tissue fibrosis : molecular signals, cellular mechanisms and translational implications", Mol Aspects Med, 65, pp.2~15 (2019)
  4. Rieder F, "An expert consensus to standardise definitions, diagnosis and treatment targets for anti-fibrotic stricture therapies in Crohn's disease", Aliment Pharmacol Ther, 48, pp.347~357 (2018)
  5. Rieder F, "Crohn's disease complicated by strictures : a systematic review", Gut, 62, pp.1072~1084 (2013)
  6. Gumaste V, "Benign and malignant colorectal strictures in ulcerative colitis", Gut, 33, pp.938~941 (1992)
  7. Chang JT, "Pathophysiology of inflammatory bowel diseases", N Engl J Med, 383, pp.2652~2664 (2020)
  8. Rieder F, "Mechanisms, management, and treatment of fibrosis in patients with inflammatory bowel diseases", Gastroenterology, 152, pp.340~350 (2017)
  9. Louis E, "Behaviour of Crohn's disease according to the Vienna classification : changing pattern over the course of the disease", Gut, 49, pp.777~782 (2001)
  10. Gordon IO, "Fibrosis in ulcerative colitis : mechanisms, features, and consequences of a neglected problem", Inflamm Bowel Dis, 20, pp.2198~2206 (2014)
  11. Baumgart DC, "Newer biologic and small-molecule therapies for inflammatory bowel disease", N Engl J Med, 385, pp.1302~1315 (2021)
  12. D'Alessio S, "Revisiting fibrosis in inflammatory bowel disease : the gut thickens", Nat Rev Gastroenterol Hepatol, 19, pp.169~184 (2022)
  13. Wang J, "Novel mechanisms and clinical trial endpoints in intestinal fibrosis", Immunol Rev, 302, pp.211~227 (2021)
  14. Herrera J, "Extracellular matrix as a driver of progressive fibrosis", J Clin Invest, 128, pp.45~53 (2018)
  15. Bochaton-Piallat ML, "The myofibroblast in wound healing and fibrosis : answered and unanswered questions", F1000Res, 5(F1000 Faculty Rev), pp.752~ (2016)
  16. Davidson S, "Fibroblasts as immune regulators in infection, inflammation and cancer", Nat Rev Immunol, 21, pp.704~717 (2021)
  17. West NR, "Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor-neutralizing therapy in patients with inflammatory bowel disease", Nat Med, 23, pp.579~589 (2017)
  18. Rock JR, "Multiple stromal populations contribute to pulmonary fibrosis without evidence for epithelial to mesenchymal transition", Proc Natl Acad Sci U S A, 108, pp.E1475~E1483 (2011)
  19. LeBleu VS, "Origin and function of myofibroblasts in kidney fibrosis", Nat Med, 19, pp.1047~1053 (2013)
  20. Zidar N, "Pathology of fibrosis in Crohn's disease-contribution to understanding its pathogenesis", Front Med(Lausanne), 7, pp.167~ (2020)
  21. Driskell RR, "Distinct fibroblast lineages determine dermal architecture in skin development and repair", Nature, 504, pp.277~281 (2013)
  22. Wynn TA, "Cellular and molecular mechanisms of fibrosis", J Pathol, 214, pp.199~210 (2008)
  23. Krystel-Whittemore M, "Mast cell : a multi-functional master cell", Front Immunol, 6, pp.620~ (2016)
  24. Galdiero MR, "Bidirectional mast cell-eosinophil interactions in inflammatory disorders and cancer", Front Med(Lausanne), 4, pp.103~ (2017)
  25. D'Urso M, "Mechanical and physical regulation of fibroblast-myofibroblast transition : from cellular mechanoresponse to tissue pathology", Front Bioeng Biotechnol, 8, pp.609653~ (2020)
  26. Li GQ, "Celastrol inhibits interleukin-17A-stimulated rheumatoid fibroblast-like synoviocyte migration and invasion through suppression of NF-κBmediated matrix metalloproteinase-9 expression", Int Immunopharmacol, 14, pp.422~431 (2012)
  27. Lawrance IC, "Altered response of intestinal mucosal fibroblasts to profibrogenic cytokines in inflammatory bowel disease", Inflamm Bowel Dis, 7, pp.226~236 (2001)
  28. Wohlfahrt T, "PU. 1 controls fibroblast polarization and tissue fibrosis", Nature, 566, pp.344~349 (2019)
  29. Muhl L, "Single-cell analysis uncovers fibroblast heterogeneity and criteria for fibroblast and mural cell identification and discrimination", Nat Commun, 11, pp.3953~ (2020)
  30. Baum J, "Fibroblasts and myofibroblasts : what are we talking about?", J Cardiovasc Pharmacol, 57, pp.376~379 (2011)
  31. Rieder F, "Wound healing and fibrosis in intestinal disease", Gut, 56, pp.130~139 (2007)
  32. Lawrance IC, "Cellular and molecular mediators of intestinal fibrosis", J Crohns Colitis, 11, pp.1491~1503 (2017)
  33. Rieder F, "Intestinal fibrosis in IBD : a dynamic, multifactorial process", Nat Rev Gastroenterol Hepatol, 6, pp.228~235 (2009)
  34. Klingberg F, "The myofibroblast matrix : implications for tissue repair and fibrosis", J Pathol, 229, pp.298~309 (2013)
  35. Li C, "The fate of myofibroblasts during the development of fibrosis in Crohn's disease", J Dig Dis, 21, pp.326~331 (2020)
  36. Li C, "Increased activation of latent TGF-β1 by αVβ3 in human Crohn's disease and fibrosis in TNBS colitis can be prevented by cilengitide", Inflamm Bowel Dis, 19, pp.2829~2839 (2013)
  37. Frangogiannis N, "Transforming growth factor-β in tissue fibrosis", J Exp Med, 217, pp.e20190103~ (2020)
  38. de Bruyn JR, "Fibrostenotic phenotype of myofibroblasts in Crohn’s disease is dependent on tissue stiffness and reversed by LOX inhibition", J Crohns Colitis, 12, pp.849~859 (2018)
  39. Kobayashi M, "Bioengineering functional smooth muscle with spontaneous rhythmic contraction in vitro", Sci Rep, 8, pp.13544~ (2018)
  40. Allahverdian S, "Smooth muscle cell fate and plasticity in atherosclerosis", Cardiovasc Res, 114, pp.540~550 (2018)
  41. Severi C, "Contribution of intestinal smooth muscle to Crohn's disease fibrogenesis", Eur J Histochem, 58, pp.2457~ (2014)
  42. Ng EK, "Human intestinal epithelial and smooth muscle cells are potent producers of IL-6", Mediators Inflamm, 12, pp.3~8 (2003)
  43. Kalluri R, "Epithelial-mesenchymal transition and its implications for fibrosis", J Clin Invest, 112, pp.1776~1784 (2003)
  44. Lovisa S, "Role of epithelial-to-mesenchymal transition in inflammatory bowel disease", J Crohns Colitis, 13, pp.659~668 (2019)
  45. Di Gregorio J, "The epithelial-tomesenchymal transition as a possible therapeutic target in fibrotic disorders", Front Cell Dev Biol, 8, pp.607483~ (2020)
  46. Flier SN, "Identification of epithelial to mesenchymal transition as a novel source of fibroblasts in intestinal fibrosis", J Biol Chem, 285, pp.20202~20212 (2010)
  47. Bataille F, "Evidence for a role of epithelial mesenchymal transition during pathogenesis of fistulae in Crohn's disease", Inflamm Bowel Dis, 14, pp.1514~1527 (2008)
  48. Ortiz-Masià D, "WNT2b activates epithelial-mesenchymal transition through FZD4 : relevance in penetrating Crohn´s disease", J Crohns Colitis, 14, pp.230~239 (2020)
  49. Iwano M, "Evidence that fibroblasts derive from epithelium during tissue fibrosis", J Clin Invest, 110, pp.341~350 (2002)
  50. Frid MG, "Mature vascular endothelium can give rise to smooth muscle cells via endothelialmesenchymal transdifferentiation : in vitro analysis", Circ Res, 90, pp.1189~1196 (2002)
  51. Zhang Y, "Endothelial to mesenchymal transition contributes to arsenic-trioxide-induced cardiac fibrosis", Sci Rep, 6, pp.33787~ (2016)
  52. Rieder F, "Inflammation-induced endothelial-to-mesenchymal transition : a novel mechanism of intestinal fibrosis", Am J Pathol, 179, pp.2660~2673 (2011)
  53. Santamaria PG, "EMT : present and future in clinical oncology", Mol Oncol, 11, pp.718~738 (2017)
  54. Vannucchi MG, "Telocytes express PDGFRα in the human gastrointestinal tract", J Cell Mol Med, 17, pp.1099~1108 (2013)
  55. Milia AF, "Telocytes in Crohn's disease", J Cell Mol Med, 17, pp.1525~1536 (2013)
  56. Ibba-Manneschi L, "Telocyte implications in human pathology : an overview", Semin Cell Dev Biol, 55, pp.62~69 (2016)
  57. Wollheim FA, "Telocytes, communicators in healthy stroma and relation to inflammation and fibrosis", Joint Bone Spine, 83, pp.615~618 (2016)
  58. Manetti M, "Telocytes are reduced during fibrotic remodelling of the colonic wall in ulcerative colitis", J Cell Mol Med, 19, pp.62~73 (2015)
  59. Sahebally SM, "Circulating fibrocytes and Crohn's disease", Br J Surg, 100, pp.1549~1556 (2013)
  60. Mifflin RC, "Intestinal myofibroblasts : targets for stem cell therapy", Am J Physiol Gastrointest Liver Physiol, 300, pp.G684~G696 (2011)
  61. Sazuka S, "Fibrocytes are involved in inflammation as well as fibrosis in the pathogenesis of Crohn's disease", Dig Dis Sci, 59, pp.760~768 (2014)
  62. Grieb G, "Circulating fibrocytes : biology and mechanisms in wound healing and scar formation", Int Rev Cell Mol Biol, 291, pp.1~19 (2011)
  63. Ueno A, "Association of circulating fibrocytes with fibrostenotic small bowel Crohn's disease", Inflamm Bowel Dis, 28, pp.246~258 (2022)
  64. Kuroda N, "Infiltrating CCR2+monocytes and their progenies, fibrocytes, contribute to colon fibrosis by inhibiting collagen degradation through the production of TIMP-1", Sci Rep, 9, pp.8568~ (2019)
  65. Friedrich M, "Cytokine networks in the pathophysiology of inflammatory bowel disease", Immunity, 50, pp.992~1006 (2019)
  66. Gieseck RL 3rd, "Type 2 immunity in tissue repair and fibrosis", Nat Rev Immunol, 18, pp.62~76 (2018)
  67. Pelly VS, "IL-4-producing ILC2s are required for the differentiation of TH2 cells following Heligmosomoides polygyrus infection", Mucosal Immunol, 9, pp.1407~1417 (2016)
  68. Gibbs BF, "Purified human peripheral blood basophils release interleukin-13 and preformed interleukin-4 following immunological activation", Eur J Immunol, 26, pp.2493~2498 (1996)
  69. Symowski C, "Th2 cell-derived IL-4", IL-13promote ILC2 accumulation in the lung by ILC2-intrinsic STAT6 signaling in mice, 2019, pp.49, 1421~1432
  70. Gordon S, "Alternative activation of macrophages : mechanism and functions", Immunity, 32, pp.593~604 (2010)
  71. Barron L, "Fibrosis is regulated by Th2 and Th17responses and by dynamic interactions between fibroblasts and macrophages", Am J Physiol Gastrointest Liver Physiol, 300, pp.G723~G728 (2011)
  72. Wynn TA, "Fibrotic disease and the T(H)1", T(H)2 paradigm, 2004, pp.4, 583~594
  73. Maher TM, "Phase 2 trial to assess lebrikizumab in patients with idiopathic pulmonary fibrosis", Eur Respir J, 57, pp.1902442~ (2021)
  74. Raghu G, "SAR156597 in idiopathic pulmonary fibrosis : a phase 2 placebo-controlled study(DRI11772)", Eur Respir J, 52, pp.1801130~ (2018)
  75. Raghu G, "A placebo-controlled trial of interferon gamma-1b in patients with idiopathic pulmonary fibrosis", N Engl J Med, 350, pp.125~133 (2004)
  76. Allanore Y, "A randomised, double-blind, placebo-controlled, 24-week, phase II, proof-ofconcept study of romilkimab(SAR156597)in early diffuse cutaneous systemic sclerosis", Ann Rheum Dis, 79, pp.1600~1607 (2020)
  77. Wynn TA, "Macrophages in tissue repair, regeneration, and fibrosis", Immunity, 44, pp.450~462 (2016)
  78. Cosín-Roger J, "The activation of Wnt signaling by a STAT6-dependent macrophage phenotype promotes mucosal repair in murine IBD", Mucosal Immunol, 9, pp.986~998 (2016)
  79. Dharmasiri S, "Human intestinal macrophages are involved in the pathology of both ulcerative colitis and Crohn disease", Inflamm Bowel Dis, 27, pp.1641~1652 (2021)
  80. Salvador P, "CD16+ macrophages mediate fibrosis in inflammatory bowel disease", J Crohns Colitis, 12, pp.589~599 (2018)
  81. Nayar S, "A myeloid-stromal niche and gp130 rescue in NOD2-driven Crohn's disease", Nature, 593, pp.275~281 (2021)
  82. Aran D, "Reference-based analysis of lung single-cell sequencing reveals a transitional profibrotic macrophage", Nat Immunol, 20, pp.163~172 (2019)
  83. Patel DD, "Th17 cell pathway in human immunity : lessons from genetics and therapeutic interventions", Immunity, 43, pp.1040~1051 (2015)
  84. Ramani K, "Interleukin-17 : friend or foe in organ fibrosis", Cytokine, 120, pp.282~288 (2019)
  85. Biancheri P, "The role of interleukin 17 in Crohn's disease-associated intestinal fibrosis", Fibrogenesis Tissue Repair, 6, pp.13~ (2013)
  86. Honzawa Y, "Involvement of interleukin-17A-induced expression of heat shock protein 47in intestinal fibrosis in Crohn's disease", Gut, 63, pp.1902~1912 (2014)
  87. Brockmann L, "Regulation of TH17 cells and associated cytokines in wound healing, tissue regeneration, and carcinogenesis", Int J Mol Sci, 18, pp.1033~ (2017)
  88. Paul J, "IL-17-driven intestinal fibrosis is inhibited by Itch-mediated ubiquitination of HIC-5", Mucosal Immunol, 11, pp.427~436 (2018)
  89. Zhang HJ, "IL-17A promotes initiation and development of intestinal fibrosis through EMT", Dig Dis Sci, 63, pp.2898~2909 (2018)
  90. Li J, "Role of interleukin-17 in pathogenesis of intestinal fibrosis in mice", Dig Dis Sci, 65, pp.1971~1979 (2020)
  91. Hueber W, "Secukinumab, a human anti-IL-17A monoclonal antibody, for moderate to severe Crohn's disease : unexpected results of a randomised, double-blind placebo-controlled trial", Gut, 61, pp.1693~1700 (2012)
  92. Targan SR, "A randomized, double-blind, placebo-controlled phase 2 study of brodalumab in patients with moderate-to-severe Crohn's disease", Am J Gastroenterol, 111, pp.1599~1607 (2016)
  93. McGee HM, "IL-22 promotes fibroblast-mediated wound repair in the skin", J Invest Dermatol, 133, pp.1321~1329 (2013)
  94. Liang SC, "Interleukin(IL)-22and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides", J Exp Med, 203, pp.2271~2279 (2006)
  95. Klose CS, "Innate lymphoid cells as regulators of immunity, inflammation and tissue homeostasis", Nat Immunol, 17, pp.765~774 (2016)
  96. Eberl G, "Innate lymphoid cells. Innate lymphoid cells: a new paradigm in immunology", Science, 348, pp.aaa6566~ (2015)
  97. Klose C, "Differentiation of type 1ILCs from a common progenitor to all helper-like innate lymphoid cell lineages", Cell, 157, pp.340~356 (2014)
  98. Kabata H, "The group 2 innate lymphoid cell(ILC2)regulatory network and its underlying mechanisms", Immunol Rev, 286, pp.37~52 (2018)
  99. Gladiator A, "Cutting edge : IL-17-secreting innate lymphoid cells are essential for host defense against fungal infection", J Immunol, 190, pp.521~525 (2013)
  100. Zheng Y, "Interleukin-22mediates early host defense against attaching and effacing bacterial pathogens", Nat Med, 14, pp.282~289 (2008)
  101. Messing M, "Group 2 innate lymphoid cells : central players in a recurring theme of repair and regeneration", Int J Mol Sci, 21, pp.1350~ (2020)
  102. Forkel M, "Distinct alterations in the composition of mucosal innate lymphoid cells in newly diagnosed and established Crohn’s disease and ulcerative colitis", J Crohns Colitis, 13, pp.67~78 (2019)
  103. Lo BC, "The orphan nuclear receptor RORα and group 3 innate lymphoid cells drive fibrosis in a mouse model of Crohn's disease", Sci Immunol, 1, pp.eaaf8864~ (2016)
  104. Scarpa M, "The epithelial danger signal IL-1α is a potent activator of fibroblasts and reactivator of intestinal inflammation", Am J Pathol, 185, pp.1624~1637 (2015)
  105. Drygiannakis I, "Proinflammatory cytokines induce crosstalk between colonic epithelial cells and subepithelial myofibroblasts : implication in intestinal fibrosis", J Crohns Colitis, 7, pp.286~300 (2013)
  106. Okuno T, "Interleukin-1beta and tumor necrosis factor-alpha induce chemokine and matrix metalloproteinase gene expression in human colonic subepithelial myofibroblasts", Scand J Gastroenterol, 37, pp.317~324 (2002)
  107. Andoh A, "Interleukin(IL)-4 and IL-17 synergistically stimulate IL-6 secretion in human colonic myofibroblasts", Int J Mol Med, 10, pp.631~634 (2002)
  108. Dohi T, "Mice deficient in Th1-and Th2-type cytokines develop distinct forms of hapten-induced colitis", Gastroenterology, 119, pp.724~733 (2000)
  109. Li C, "Noncanonical STAT3 activation regulates excess TGF-β1 and collagen I expression in muscle of stricturing Crohn's disease", J Immunol, 194, pp.3422~3431 (2015)
  110. Franzè E, "Cadherin-11 is a regulator of intestinal fibrosis", J Crohns Colitis, 14, pp.406~417 (2020)
  111. Li C, "Mechanisms that mediate the development of fibrosis in patients with Crohn's disease", Inflamm Bowel Dis, 20, pp.1250~1258 (2014)
  112. Theiss AL, "Growth hormone reduces the severity of fibrosis associated with chronic intestinal inflammation", Gastroenterology, 129, pp.204~219 (2005)
  113. Rogler G, "Differential activation of cytokine secretion in primary human colonic fibroblast", myofibroblast cultures, 2001, pp.36, 389~398
  114. Lim WW, "Transgenic interleukin 11 expression causes cross-tissue fibro-inflammation and an inflammatory bowel phenotype in mice", PLoS One, 15, pp.e0227505~ (2020)
  115. Guan Q, "Targeting IL-12", IL-23by employing a p40 peptide-based vaccine ameliorates TNBS-induced acute and chronic murine colitis, 2011, pp.17, 646~656
  116. Guan Q, "Reversing ongoing chronic intestinal inflammation and fibrosis by sustained block of IL-12 and IL-23 using a vaccine in mice", Inflamm Bowel Dis, 24, pp.1941~1952 (2018)
  117. Fichtner-Feigl S, "Induction of IL-13 triggers TGF-beta1-dependent tissue fibrosis in chronic 2, 4, 6-trinitrobenzene sulfonic acid colitis", J Immunol, 178, pp.5859~5870 (2007)
  118. Fichtner-Feigl S, "IL-13 signaling via IL-13R alpha2 induces major downstream fibrogenic factors mediating fibrosis in chronic TNBS colitis", Gastroenterology, 135, pp.2003~2013 (2008)
  119. Yagi Y, "Inflammatory responses induced by interleukin-17 family members in human colonic subepithelial myofibroblasts", J Gastroenterol, 42, pp.746~753 (2007)
  120. Speca S, "Cellular and molecular mechanisms of intestinal fibrosis", World J Gastroenterol, 18, pp.3635~3661 (2012)
  121. Monteleone G, "Control of matrix metalloproteinase production in human intestinal fibroblasts by interleukin 21", Gut, 55, pp.1774~1780 (2006)
  122. Zenewicz LA, "Innate and adaptive interleukin-22protects mice from inflammatory bowel disease", Immunity, 29, pp.947~957 (2008)
  123. Andoh A, "Interleukin-22, a member of the IL-10 subfamily, induces inflammatory responses in colonic subepithelial myofibroblasts", Gastroenterology, 129, pp.969~984 (2005)
  124. Mathur R, "Induction of autophagy in Cx3cr1+ mononuclear cells limits IL-23", IL-22 axismediated intestinal fibrosis, 2019, pp.12, 612~623
  125. Borowczyk J, "IL-25(IL-17E)in epithelial immunology and pathophysiology", J Allergy Clin Immunol, 148, pp.40~52 (2021)
  126. Wang AJ, "Genetic deletion of IL-25(IL-17E)confers resistance to dextran sulfate sodium-induced colitis in mice", Cell Biosci, 4, pp.72~ (2014)
  127. Imai J, "Flagellin-mediated activation of IL-33-ST2 signaling by a pathobiont promotes intestinal fibrosis", Mucosal Immunol, 12, pp.632~643 (2019)
  128. Kotsiou OS, "IL-33", ST2axis in organ fibrosis, 2018, pp.9, 2432~
  129. Franzè E, "Interleukin-34 stimulates gut fibroblasts to produce collagen synthesis", J Crohns Colitis, 14, pp.1436~1445 (2020)
  130. Scheibe K, "Inhibiting interleukin 36 receptor signaling reduces fibrosis in mice with chronic intestinal inflammation", Gastroenterology, 156, pp.1082~1097 (2019)
  131. Shih DQ, "Inhibition of a novel fibrogenic factor Tl1a reverses established colonic fibrosis", Mucosal Immunol, 7, pp.1492~1503 (2014)
  132. Wenxiu J, "Effect and mechanism of TL1A expression on epithelial-mesenchymal transition during chronic colitis-related intestinal fibrosis", Mediators Inflamm, 2021, pp.5927064~ (2021)
  133. Ulloa L, "Inhibition of transforming growth factor-beta", SMAD signalling by the interferongamma, Nature, pp.1999, 397[DOI]
  134. Leeb SN, "Reduced migration of fibroblasts in inflammatory bowel disease : role of inflammatory mediators and focal adhesion kinase", Gastroenterology, 125, pp.1341~1354 (2003)
  135. Francoeur C, "Degeneration of the pericryptal myofibroblast sheath by proinflammatory cytokines in inflammatory bowel diseases", Gastroenterology, 136, pp.268~277 (2009)
  136. Kobori A, "Interleukin-33 expression is specifically enhanced in inflamed mucosa of ulcerative colitis", J Gastroenterol, 45, pp.999~1007 (2010)
  137. Lopetuso LR, "IL-33 promotes recovery from acute colitis by inducing miR-320 to stimulate epithelial restitution and repair", Proc Natl Acad Sci U S A, 115, pp.E9362~E9370 (2018)
  138. Masterson JC, "Eosinophils and IL-33 perpetuate chronic inflammation and fibrosis in a pediatric population with stricturing Crohn's ileitis", Inflamm Bowel Dis, 21, pp.2429~2440 (2015)
  139. Lu W, "Platelet-derived growth factor C signaling is a potential therapeutic target for radiation proctopathy", Sci Transl Med, 13, pp.eabc2344~ (2021)
  140. Takemura N, "Eosinophil depletion suppresses radiation-induced small intestinal fibrosis", Sci Transl Med, 10, pp.eaan0333~ (2018)
  141. Walana W, "IL-8 antagonist, CXCL8(3-72)K11R", G31P coupled with probiotic exhibit variably enhanced therapeutic potential in ameliorating ulcerative colitis, 2018, pp.103, 253~261
  142. Lenti MV, "Intestinal fibrosis", Mol Aspects Med, 65, pp.100~109 (2019)
  143. Cook SA, "Hiding in plain sight : interleukin-11emerges as a master regulator of fibrosis, tissue integrity, and stromal inflammation", Annu Rev Med, 71, pp.263~276 (2020)
  144. Ng B, "Interleukin-11 is a therapeutic target in idiopathic pulmonary fibrosis", Sci Transl Med, 11, pp.eaaw1237~ (2019)
  145. Schafer S, "IL-11 is a crucial determinant of cardiovascular fibrosis", Nature, 552, pp.110~115 (2017)
  146. Martin JC, "Single-cell analysis of Crohn’s disease lesions identifies a pathogenic cellular module associated with resistance to anti-TNF therapy", Cell, 178, pp.1493~1508 (2019)
  147. Schmitz J, "IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines", Immunity, 23, pp.479~490 (2005)
  148. Lopetuso LR, "Emerging role of the interleukin(IL)-33", ST2 axis in gut mucosal wound healing and fibrosis, 2012, pp.5, 18~
  149. Morimoto Y, "Amphiregulinproducing pathogenic memory T helper 2 cells instruct eosinophils to secrete osteopontin and facilitate airway fibrosis", Immunity, 49, pp.134~150 (2018)
  150. Baghdadi M, "Interleukin-34, a comprehensive review", J Leukoc Biol, 104, pp.931~951 (2018)
  151. Preisser L, "IL-34and macrophage colony-stimulating factor are overexpressed in hepatitis C virus fibrosis and induce profibrotic macrophages that promote collagen synthesis by hepatic stellate cells", Hepatology, 60, pp.1879~1890 (2014)
  152. Baek JH, "IL-34 mediates acute kidney injury and worsens subsequent chronic kidney disease", J Clin Invest, 125, pp.3198~3214 (2015)
  153. Franzè E, "Interleukin-34sustains inflammatory pathways in the gut", Clin Sci(Lond), 129, pp.271~280 (2015)
  154. Zwicker S, "Interleukin 34: a new modulator of human and experimental inflammatory bowel disease", Clin Sci(Lond), 129, pp.281~290 (2015)
  155. Hwang SJ, "Interleukin-34 produced by human fibroblast-like synovial cells in rheumatoid arthritis supports osteoclastogenesis", Arthritis Res Ther, 14, pp.R14~ (2012)
  156. Mantovani A, "Interleukin-1 and related cytokines in the regulation of inflammation and immunity", Immunity, 50, pp.778~795 (2019)
  157. Elias M, "IL-36 in chronic inflammation and fibrosis: bridging the gap?", J Clin Invest, 131, pp.e144336~ (2021)
  158. Nishida A, "Increased expression of interleukin-36, a member of the interleukin-1 cytokine family, in inflammatory bowel disease", Inflamm Bowel Dis, 22, pp.303~314 (2016)
  159. Scheibe K, "IL-36R signalling activates intestinal epithelial cells and fibroblasts and promotes mucosal healing in vivo", Gut, 66, pp.823~838 (2017)
  160. Takahashi K, "Interleukin(IL)-1βis a strong inducer of IL-36γ expression in human colonic myofibroblasts", PLoS One, 10, pp.e0138423~ (2015)
  161. Migone TS, "TL1A is a TNF-like ligand for DR3 and TR6", DcR3 and functions as a T cell costimulator, 2002, pp.16, 479~492
  162. Valatas V, "TL1A(TNFSF15)and DR3(TNFRSF25) : a co-stimulatory system of cytokines with diverse functions in gut mucosal immunity", Front Immunol, 10, pp.583~ (2019)
  163. Takedatsu H, "TL1A(TNFSF15)regulates the development of chronic colitis by modulating both T-helper 1 and T-helper 17 activation", Gastroenterology, 135, pp.552~567 (2008)
  164. Jacob N, "Direct signaling of TL1A-DR3 on fibroblasts induces intestinal fibrosis in vivo", Sci Rep, 10, pp.18189~ (2020)
  165. Li H, "TL1A blocking ameliorates intestinal fibrosis in the T cell transfer model of chronic colitis in mice", Pathol Res Pract, 214, pp.217~227 (2018)
  166. Barrett R, "Constitutive TL1A expression under colitogenic conditions modulates the severity and location of gut mucosal inflammation and induces fibrostenosis", Am J Pathol, 180, pp.636~649 (2012)
  167. Yang DH, "TNFSF15 is an independent predictor for the development of Crohn's disease-related complications in Koreans", J Crohns Colitis, 8, pp.1315~1326 (2014)
  168. Shih DQ, "Constitutive TL1A(TNFSF15)expression on lymphoid or myeloid cells leads to mild intestinal inflammation and fibrosis", PLoS One, 6, pp.e16090~ (2011)
  169. Clarke AW, "An anti-TL1A antibody for the treatment of asthma and inflammatory bowel disease", MAbs, 10, pp.664~677 (2018)
  170. Jacob N, "Inflammation-independent TL1A-mediated intestinal fibrosis is dependent on the gut microbiome", Mucosal Immunol, 11, pp.1466~1476 (2018)
  171. Hassan-Zahraee M, "Antitumor necrosis factor-like ligand 1A therapy targets tissue inflammation and fibrosis pathways and reduces gut pathobionts in ulcerative colitis", Inflamm Bowel Dis, 28, pp.434~446 (2022)
  172. Li J, "Pathogenesis of fibrostenosing Crohn's disease", Transl Res, 209, pp.39~54 (2019)
  173. Bos S, "Metabolic modulation during intestinal fibrosis", J Dig Dis, 21, pp.319~325 (2020)
  174. Latella G, "Results of the 4th scientific workshop of the ECCO(I) : pathophysiology of intestinal fibrosis in IBD", J Crohns Colitis, 8, pp.1147~1165 (2014)
  175. Derkacz A, "The role of extracellular matrix components in inflammatory bowel diseases", J Clin Med, 10, pp.1122~ (2021)
  176. Soroosh A, "Crohn's disease fibroblasts overproduce the novel protein KIAA1199 to create proinflammatory hyaluronan fragments", Cell Mol Gastroenterol Hepatol, 2, pp.358~368 (2016)
  177. Wight TN, "The extracellular matrix: an active or passive player in fibrosis?", Am J Physiol Gastrointest Liver Physiol, 301, pp.G950~G955 (2011)
  178. Flynn RS, "Endogenous IGF-I and alphaVbeta3 integrin ligands regulate increased smooth muscle hyperplasia in stricturing Crohn's disease", Gastroenterology, 138, pp.285~293 (2010)
  179. Sheehan AL, "Fat-wrapping in Crohn's disease : pathological basis and relevance to surgical practice", Br J Surg, 79, pp.955~958 (1992)
  180. Borley NR, "The relationship between inflammatory and serosal connective tissue changes in ileal Crohn's disease : evidence for a possible causative link", J Pathol, 190, pp.196~202 (2000)
  181. Liu Q, "Constrictive and hypertrophic strictures in ileal Crohn's disease", Clin Gastroenterol Hepatol, 20, pp.e1292~e1304 (2022)
  182. Coffey CJ, "Inclusion of the mesentery in ileocolic resection for Crohn's disease is associated with reduced surgical recurrence", J Crohns Colitis, 12, pp.1139~1150 (2018)
  183. Ha C, "Translocation of viable gut microbiota to mesenteric adipose drives formation of creeping fat in humans", Cell, 183, pp.666~683 (2020)
  184. Mao R, "A positive feedback loop between creeping fat and intestinal stricture formation in Crohn's disease : the role of creeping fat-derived free fatty acids, extracellular matrix, and integrin", Gastroenterology, 158, pp.S-188~S-189 (2020)
  185. Mao R, "Creeping-fat derived free fatty acids induce hyperplasia of intestinal muscularis propria muscle cells : a novel link between fat and intestinal stricture formation in Crohn's disease", Gastroenterology, 154, pp.S-131~ (2018)
  186. Mao R, "Activated intestinal muscle cells promote preadipocyte migration : a novel mechanism for creeping fat formation in Crohn's disease", Gut, 71, pp.55~67 (2022)
  187. Bauer-Rowe KE, "Where there is fat there is fibrosis : elucidating the mechanisms of creeping fatdriven stricture formation", J Am Coll Surg, 233, pp.S65~ (2021)
  188. Xiong S, "Reverse translation approach generates a signature of penetrating fibrosis in Crohn's disease that is associated with anti-TNF response", Gut, 71, pp.1289~1301 (2022)
  189. Bauer-Rowe KE, "A Surgical model for investigating the role of creeping fat in intestinal fibrosis", J Am Coll Surg, 231, pp.S50~S51 (2020)
  190. Rieder F, "The gut microbiome in intestinal fibrosis : environmental protector or provocateur?", Sci Transl Med, 5, pp.190ps10~ (2013)
  191. Darfeuille-Michaud A, "High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn's disease", Gastroenterology, 127, pp.412~421 (2004)
  192. Zorzi F, "Pathogenic aspects and therapeutic avenues of intestinal fibrosis in Crohn's disease", Clin Sci(Lond), 129, pp.1107~1113 (2015)
  193. Sugiura H, "Activation of Tolllike receptor 3 augments myofibroblast differentiation", Am J Respir Cell Mol Biol, 40, pp.654~662 (2009)
  194. Bhattacharyya S, "Pharmacological inhibition of Toll-like receptor-4 signaling by TAK242 prevents and induces regression of experimental organ fibrosis", Front Immunol, 9, pp.2434~ (2018)
  195. Yang R, "Toll-like receptor 4 contributes to a myofibroblast phenotype in cardiac fibroblasts and is associated with autophagy after myocardial infarction in a mouse model", Atherosclerosis, 279, pp.23~31 (2018)
  196. Macias-Ceja DC, "Succinate receptor mediates intestinal inflammation and fibrosis", Mucosal Immunol, 12, pp.178~187 (2019)
  197. Di Gregorio J, "Role of glycogen synthase kinase-3β and PPAR-γ on epithelial-to-mesenchymal transition in DSS-induced colorectal fibrosis", PLoS One, 12, pp.e0171093~ (2017)
  198. Mao R, "The mesenteric fat and intestinal muscle interface : creeping fat influencing stricture formation in Crohn's disease", Inflamm Bowel Dis, 25, pp.421~426 (2019)

관련 논문AI추천

Inflammatory bowel disease–associated intestinal fibrosis김정석, 박지민, 배성욱, 이유진, 이혜원대한병리학회 · Journal of Pathology and Translational Medicine2023 · 제57권 제1호Downregulation of Heat Shock Protein 72 Contributes to Fibrostenosis in Crohn’s DiseaseAhn Jae Bum, Cheon Jae Hee, Kim Duk Hwan, Kim Ji Hyung, Kim Seung Won, Lee Han Cheol, Lee Jae-Young, Park I Seul거트앤리버 소화기연관학회협의회 · Gut and Liver2023 · 제17권 제6호Inflammation and tissue remodeling contribute to fibrogenesis in stricturing Crohn’s disease: image processing and analysis study이화정, Dipti Karamchandani, Hua Li, Kyle Hodge, Lianna Goetz, Michael W. Mikula, Mustafa Erdem Arslan, Rupinder Brar, Sangtae Ahn대한병리학회 · Journal of Pathology and Translational Medicine2022 · 제56권 제5호Anti-fibrotic treatments for chronic liver diseases: The present and the futureHideki Fujii, Masaru Enomoto, Misako Sato-Matsubara, Naoshi Odagiri, Norifumi Kawada, Tsutomu Matsubara대한간학회 · Clinical and Molecular Hepatology2021 · 제27권 제3호Reversal of liver cirrhosis: current evidence and expectations임형준, 정영걸대한내과학회 · The Korean Journal of Internal Medicine2017 · 제32권 제2호Molecular Activity of Inflammation and Epithelial-Mesenchymal Transition in the Microenvironment of Ulcerative Colitis김나영, 이동호, Choi Yonghoon, Jun Yu Kyung, Kim Hyung Kyung, Lee Ji Ae, Park Ji Hyun, Park Young Soo, Shin Cheol Min, Yoon Hyuk거트앤리버 소화기연관학회협의회 · Gut and Liver2024 · 제18권 제6호

이 간행물의 다른 논문 (15건)