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Molecular and Signaling Pathways in Pathological Changes of Esophageal, Gastric...
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Molecular and Signaling Pathways in Pathological Changes of Esophageal, Gastric and Intestinal Epithelial Cells and Methods of Cell Protective Treatment

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 25 February 2026 | Viewed by 1120

Special Issue Editor

Prof. Dr. Tomasz Brzozowski

E-Mail Website
Guest Editor
Department of Physiology, Faculty of Medicine, Jagiellonian University Medical College, 31-531 Cracow, Poland
Interests: gastrointestinal physiology; gastroenterology; esophageal disorders; peptic ulcer disease; inflammatory bowel disease; ulcerative colitis; pharmacology of the gut
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of Cells is dedicated to the changes in gastrointestinal physiology and pathology of esophageal, gastric, and intestinal epithelial cells, including cell damage, as well as the methods of protecting these cells by physiological factors and pharmacological agents.

The importance of the gastrointestinal tract (GI tract) in maintaining general health is crucial not only for normal intestinal functions, such as digestion and absorption of nutrients, which are responsible for physiological growth and development of organs but also for the proper functioning of other systems in the body, including the nervous system (brain–gut axis), cardiovascular and excretory systems, as well as acid–base balance. Maintaining the proper structure and function of these cells plays a crucial role in the integrity of the GI tract, preventing the entry of harmful substances into the body. Our goal is to provide an in-depth analysis of the various types and functions of these cells in health and disease, and to explore the involvement of multiple signaling pathways in the spectrum of diseases affecting epithelial cells that are constantly exposed to harmful stimuli. We are also interested in updating our knowledge on how these epithelial cells are protected from cellular damage in health conditions and what are the current advances in pharmacological therapy for epithelial cells of the GI tract. Original basic scientific papers, translational and clinical studies, as well as comprehensive review articles, are welcome.

You may choose our Joint Special Issue in IJMS.

Prof. Dr. Tomasz Brzozowski
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gastrointestinal epithelial cells
  • cellular signaling
  • molecular pathways
  • cell damage
  • cell protection
  • esophageal integrity
  • gastric secretion
  • gastric ulcer
  • duodenal ulcer
  • intestinal digestion and absorption
  • intestinal integrity
  • inflammatory bowel disease
  • irritable bowel syndrome
  • ulcerative colitis
  • Crohn’s disease

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Published Papers (1 paper)

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Review

34 pages, 8250 KB  
Review
From Cytokines to Biomarkers: Mapping the Immunopathology of Inflammatory Bowel Disease
by Sarah Baum, Kamron Hamedi, Caroline Loftus, Gannett Loftus, Emily-Rose Zhou and Sergio Arce
Cells 2025, 14(20), 1589; https://doi.org/10.3390/cells14201589 - 13 Oct 2025
Viewed by 945
Abstract
Inflammatory bowel disease (IBD) is a chronic immune-mediated condition of the gastrointestinal tract, characterized by dysregulated inflammatory responses throughout the gastrointestinal tract. It includes two major phenotypes, Crohn’s disease (CD) and ulcerative colitis (UC), which present with varying gastrointestinal and systemic symptoms. The [...] Read more.
Inflammatory bowel disease (IBD) is a chronic immune-mediated condition of the gastrointestinal tract, characterized by dysregulated inflammatory responses throughout the gastrointestinal tract. It includes two major phenotypes, Crohn’s disease (CD) and ulcerative colitis (UC), which present with varying gastrointestinal and systemic symptoms. The pathophysiology of IBD is multifactorial including genetic predisposition, mucosal and epithelial dysfunction, environmental injury, and both innate and adaptive immune response abnormalities. Several predisposing genetic factors have been associated with IBD explaining the strong hereditary risk for both CD and UC. For example, Caspase Recruitment Domain 9 (CARD9) variant rs10781499 increases risk for IBD, while other variants are specific to either CD or UC. CD is related to loss-of-function mutations in the nucleotide oligomerization domain containing the protein 2 (NOD2) gene and Autophagy-Related 16-like 1 (ATG16L1) gene. UC risk is increased particularly in Chinese populations by the A-1661G polymorphism of the Cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene. This abnormal CTLA-4 interferes with B- and T-cell responses causing predisposition to autoimmune conditions. Previous studies suggested that IBD results from breakdown of the adaptive immune system, primarily of T-cells. However, new evidence suggests that a primary breakdown of the innate immune system in both CD and UC increases susceptibility to invasion by viruses and bacteria, with a compensatory overactivation of the adaptive immune system as a result. When this viral and microbial invasion continues, further damage is incurred, resulting in a downward cycle of further cytokine activation and epithelial damage. Released biomarkers also affect the permeability of the epithelial membrane, including lactoferrin, nitric oxide (NO), myeloperoxidase (MPO) and its activation of hypochlorous acid, matrix metalloproteinases (MMPs), especially MMP-9, omentin-1, and others. Increased macrophage and dendritic cell dysfunction, increased neutrophil activity, increased numbers of innate lymphoid cells, increased T-cells with decreased regulatory T-cells (Tregs), and changes in B-cell populations and immunoglobulin (Ig) functions are all associated with IBD. Finally, treatment of IBD has typically consisted of medical management (e.g., aminosalicylates and corticosteroids) and lifestyle modification, and surgical intervention in extreme cases. New classes of medications with more favorable side effect profiles include anti-integrin antibodies, vedolizumab, etrolizumab, and carotegrast methyl. Additionally, fecal microbiota transplant (FMT) is a newer area of research for treatment of IBD along with TNF-blockers, JAK inhibitors, and S1PR modulators. However, expense and long preparation time have limited the usefulness of FMT. Full article
(This article belongs to the Special Issue Molecular and Signaling Pathways in Pathological Changes of Esophageal, Gastric and Intestinal Epithelial Cells and Methods of Cell Protective Treatment)
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