Intestinal fibrosis

Research output: Contribution to journalArticlepeer-review


Extensive tissue fibrosis is the end-stage process of a number of chronic conditions affecting the gastrointestinal tract, including inflammatory bowel disease (Crohn's disease, ulcerative colitis), ulcerative jejunoileitis, and radiation enteritis. Fibrogenesis is a physiological, reparative process that may become harmful as a consequence of the persistence of a noxious agent, after an excessive duration of the healing process. In this case, after replacement of dead or injured cells, fibrogenesis continues to substitute normal parenchymal tissue with fibrous connective tissue, leading to uncontrolled scar formation and, ultimately, permanent organ damage, loss of function, and/or strictures. Several mechanisms have been implicated in sustaining the fibrogenic process. Despite their obvious etiological and clinical distinctions, most of the above-mentioned fibrotic disorders have in common a persistent inflammatory stimulus which sustains the production of growth factors, proteolytic enzymes, and pro-fibrogenic cytokines that activate both non-immune (i.e., myofibroblasts, fibroblasts) and immune (i.e., monocytes, macrophages, T-cells) cells, the interactions of which are crucial in the progressive tissue remodeling and destroy. Here we summarize the current status of knowledge regarding the mechanisms implicated in gut fibrosis with a clinical approach, also focusing on possible targets of antifibrogenic therapies.
Original languageEnglish
Pages (from-to)100-109
Number of pages10
JournalMolecular Aspects of Medicine
Publication statusPublished - Feb 2019


  • *Collagen
  • *Crohn's disease
  • *Extracellular matrix
  • *Myofibroblast
  • *Strictureplasty
  • *Ulcerative colitis
  • Animals
  • Biomarkers
  • Cellular Microenvironment
  • Disease Susceptibility
  • Extracellular Matrix/metabolism
  • Fibroblasts/metabolism
  • Fibrosis
  • Gene Expression Regulation
  • Humans
  • Intestinal Diseases/diagnosis/*etiology/*metabolism/therapy
  • Myofibroblasts/metabolism
  • Phenotype
  • Signal Transduction


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