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Inflammatory Bowel Disease: From Genetics to Treatment
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Inflammatory Bowel Disease: From Genetics to Treatment

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 1743

Special Issue Editor

Dr. Dalin Li

E-Mail Website
Guest Editor
Inflammatory Bowel Disease Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
Interests: Crohn's disease; inflammatory bowel diseases; ulcerative colitis

Special Issue Information

Dear Colleagues,

Inflammatory Bowel Disease (IBD) encompasses chronic inflammatory conditions of the gastrointestinal tract, including Crohn's disease and ulcerative colitis. These diseases are characterized by a complex interplay of genetic, environmental, microbial, and immune factors, leading to chronic inflammation of the gut. The relationship between genetic predisposition and the development of Inflammatory Bowel Disease (IBD), including its two main forms, Crohn's disease and ulcerative colitis. IBD is characterized by chronic inflammation of the gastrointestinal tract, and its etiology involves a complex interplay between genetic and environmental factors. Recent advancements in genome-wide association studies (GWAS) have identified numerous genetic loci associated with IBD, shedding light on the genetic predisposition to the disease. These studies have enhanced our understanding of the genetic architecture of IBD, revealing insights into the underlying biological pathways that contribute to disease susceptibility and progression. Identifying these genetic factors is crucial for developing targeted therapies and personalized medicine approaches for IBD patients. The latest research on genetic predisposition in IBD emphasizes the role of specific genetic variants and their impact on disease phenotypes. It also explores the potential of integrating genetic data with clinical and environmental information to improve disease prediction, diagnosis, and treatment strategies. By examining the genetic basis of IBD, researchers aim to uncover novel therapeutic targets and biomarkers that can lead to more effective and individualized treatment options for patients. Moreover, the issue addresses the therapeutic implications of these genetic findings, discussing current and emerging treatments for IBD. It highlights the role of biologics, small-molecule inhibitors, and other novel therapeutic strategies in managing the disease. The integration of genetic information with therapeutic approaches holds great promise.

Dr. Dalin Li
Guest Editor

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Keywords

  • genetic predisposition
  • inflammatory bowel disease
  • genome-wide association study Crohn's disease
  • ulcerative colitis
  • bowel disease

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Published Papers (2 papers)

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20 pages, 5662 KiB  
Article
PTPN2 Regulates Iron Handling Protein Expression in Inflammatory Bowel Disease Patients and Prevents Iron Deficiency in Mice
by Hillmin Lei, Ali Shawki, Alina N. Santos, Vinicius Canale, Salomon Manz, Meli’sa S. Crawford, Pritha Chatterjee, Marianne R. Spalinger, Michael Scharl and Declan F. McCole
Int. J. Mol. Sci. 2025, 26(7), 3356; https://doi.org/10.3390/ijms26073356 - 3 Apr 2025
Viewed by 341
Abstract
Anemia is the most common extraintestinal manifestation of inflammatory bowel disease (IBD). Iron deficiency is the most frequent cause of anemia in IBD; however, the mechanisms involved are still poorly understood. Here, we investigated the role of the IBD risk gene, protein tyrosine [...] Read more.
Anemia is the most common extraintestinal manifestation of inflammatory bowel disease (IBD). Iron deficiency is the most frequent cause of anemia in IBD; however, the mechanisms involved are still poorly understood. Here, we investigated the role of the IBD risk gene, protein tyrosine phosphatase non-receptor type 2 (PTPN2), in regulating iron homeostasis. Proteomic analyses were performed on serum from IBD patients genotyped for the IBD-associated loss-of-function rs1893217 PTPN2 variant. Constitutive Ptpn2 wild type (WT), heterozygous (Het), and knockout (KO) mice were analyzed for iron content, blood parameters, and expression of iron handling proteins. Iron absorption was assessed through radiotracer assays. Serum proteomic analyses revealed that the “iron homeostasis signaling pathway” was the main pathway downregulated in Crohn’s disease (CD) patients carrying the PTPN2 risk allele, independent of disease activity. Ptpn2-KO mice showed characteristics of anemia, including reduced hemoglobin concentrations along with serum and tissue iron deficiency and elevated serum hepcidin levels vs. Ptpn2-WT and Het mice. 55Fe absorption via oral gavage was significantly impaired in Ptpn2-KO mice. Correspondingly, Ptpn2-KO mice showed reduced apical membrane expression of the iron transporter DMT1. CD patients with the PTPN2 loss-of-function rs1893217 variant display alterations in serum iron handling proteins. Loss of Ptpn2 in mice caused features of anemia, including iron deficiency associated with reduced apical membrane expression of DMT1. These findings identify an important role for PTPN2 in regulating systemic iron homeostasis. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: From Genetics to Treatment)
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Review

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67 pages, 865 KiB  
Review
Pharmacogenetics in Response to Biological Agents in Inflammatory Bowel Disease: A Systematic Review
by Octavio Ballesta-López, Mayte Gil-Candel, María Centelles-Oria, Juan Eduardo Megías-Vericat, Antonio Solana-Altabella, Hugo Ribes-Artero, Pilar Nos-Mateu, Javier García-Pellicer and José Luis Poveda-Andrés
Int. J. Mol. Sci. 2025, 26(4), 1760; https://doi.org/10.3390/ijms26041760 - 19 Feb 2025
Viewed by 815
Abstract
Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders influenced by microbial, environmental, genetic, and immune factors. The introduction of biological agents has transformed IBD therapy, improving symptoms, reducing complications, and enhancing patients’ quality of life. However, approximately 30% of patients exhibit primary non-response, [...] Read more.
Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders influenced by microbial, environmental, genetic, and immune factors. The introduction of biological agents has transformed IBD therapy, improving symptoms, reducing complications, and enhancing patients’ quality of life. However, approximately 30% of patients exhibit primary non-response, and 50% experience a loss of response over time. Genetic and non-genetic factors contribute to variability in treatment outcomes. This systematic review aims to thoroughly analyze and assess existing studies exploring the relationships between genetic variations and individual responses to biologic drugs, in order to identify genetic markers that are predictive of treatment efficacy, risk of adverse effects, or drug toxicity, thereby informing clinical practice and guiding future research. PubMed and EMBASE papers were reviewed by three independent reviewers according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses [PRISMA] guidelines. Of the 883 records screened, 99 met the inclusion criteria. The findings of this review represent an initial step toward personalized medicine in IBD, with the potential to improve clinical outcomes in biological therapy. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: From Genetics to Treatment)
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