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Inflammatory Diseases: From a Molecular Perspective

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 March 2025) | Viewed by 923

Special Issue Editor


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Guest Editor
Biomedicine and Biotechnology, Technical University of Denmark, 2800 Kongens Lyngby, Denmark
Interests: dermatology; collagens; biomarkers; inflammatory skin disease; atopic dermatitis; hidradenitis suppurativa

Special Issue Information

Dear Colleagues,

Inflammatory diseases encompass a wide range of health conditions that can affect various organs in the body. These conditions include rheumatoid arthritis (RA), spondyloarthritis (SpA), hidradenitis suppurativa (HS), inflammatory bowel disease (IBD), asthma, and autoimmune neurological disorders. While these diseases share some common features, they each impact different organs due to distinct underlying molecular processes.

The goal of this special issue, titled 'Inflammatory Diseases: From a Molecular Perspective', is to spotlight the ongoing research efforts aimed at gaining a deeper understanding of the mechanisms behind these diseases. This research seeks to identify potential therapeutic targets, explore the role of new molecular treatment options, and develop molecular diagnostic strategies that can contribute to the advancement of personalized medicine.

This special issue aims to bridge the gap between basic scientific investigations and translational research. The ultimate aim is to enhance our comprehension of the molecular mechanisms involved in inflammatory diseases.

We hope this Special Issue will be of interest to you.

Dr. Signe Holm Nielsen
Guest Editor

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Keywords

  • inflammatory diseases
  • disease mechanisms
  • diagnosis
  • therapeutic targets
  • personalized medicine

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Published Papers (1 paper)

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12 pages, 2868 KiB  
Article
miR-369-3p Ameliorates Inflammation and Apoptosis in Intestinal Epithelial Cells via the MEK/ERK Signaling Pathway
by Viviana Scalavino, Emanuele Piccinno, Gianluigi Giannelli and Grazia Serino
Int. J. Mol. Sci. 2025, 26(9), 4288; https://doi.org/10.3390/ijms26094288 - 1 May 2025
Cited by 2 | Viewed by 484
Abstract
Inflammatory Bowel Disease (IBD) is a group of chronic and recurrent inflammatory diseases characterized by prolonged inflammation of the intestinal tract. Although it has been proven that the immune system plays a crucial role in the pathogenesis of IBD, a defective intestinal epithelium [...] Read more.
Inflammatory Bowel Disease (IBD) is a group of chronic and recurrent inflammatory diseases characterized by prolonged inflammation of the intestinal tract. Although it has been proven that the immune system plays a crucial role in the pathogenesis of IBD, a defective intestinal epithelium is also responsible for chronic inflammation, hence causing an over-activation of the immune response. For this reason, a therapeutic approach that acts by improving impaired intestinal homeostasis could ensure a greater therapeutic efficacy in IBD. Mitogen-activated protein kinases (MAPKs) signaling pathways may be involved in the pathogenesis of IBD. It has been demonstrated that the inhibition of mitogen-activated protein kinase kinase 1 (MEK1) may be a potential treatment against IBD since it may restore the normal epithelial function and reduce apoptosis of intestinal epithelial cells (IECs). New therapeutic strategies are emerging including small molecules such as microRNAs (miRNAs). In this study, we aimed to demonstrate that miR-369-3p was able to modulate the MEK/ERK signaling pathway. As reported by in silico analysis, miR-369-3p was capable of pairing the 3’UTR of the MAP2K1 gene. In vitro analysis demonstrated that mimic transfection with miR-369-3p in epithelial cells downregulated the expression of MEK1, reduced the activation of ERK signaling, and modulated apoptosis of epithelial cells in response to TNF-α. Moreover, miR-369-3p significantly decreased the release of pro-inflammatory cytokine IL-8. These results support the potential of miR-369-3p to prevent apoptosis of IECs, responsible for a persistent inflammatory condition in IBD, highlighting its application value in the treatment of inflammatory disorders. Full article
(This article belongs to the Special Issue Inflammatory Diseases: From a Molecular Perspective)
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