The role of mesenchymal stem cells in attenuating inflammatory bowel disease through ubiquitination

Front Immunol. 2024 Aug 9:15:1423069. doi: 10.3389/fimmu.2024.1423069. eCollection 2024.

Abstract

Inflammatory bowel disease (IBD), a condition of the digestive tract and one of the autoimmune diseases, is becoming a disease of significant global public health concern and substantial clinical burden. Various signaling pathways have been documented to modulate IBD, but the exact activation and regulatory mechanisms have not been fully clarified; thus, a need for constant exploration of the molecules and pathways that play key roles in the development of IBD. In recent years, several protein post-translational modification pathways, such as ubiquitination, phosphorylation, methylation, acetylation, and glycolysis, have been implicated in IBD. An aberrant ubiquitination in IBD is often associated with dysregulated immune responses and inflammation. Mesenchymal stem cells (MSCs) play a crucial role in regulating ubiquitination modifications through the ubiquitin-proteasome system, a cellular machinery responsible for protein degradation. Specifically, MSCs have been shown to influence the ubiquitination of key signaling molecules involved in inflammatory pathways. This paper reviews the recent research progress in MSC-regulated ubiquitination in IBD, highlighting their therapeutic potential in treating IBD and offering a promising avenue for developing targeted interventions to modulate the immune system and alleviate inflammatory conditions.

Keywords: exosome; inflammatory bowel disease; mesenchymal stem cell; post-translational modification; ubiquitination.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Inflammatory Bowel Diseases* / immunology
  • Inflammatory Bowel Diseases* / metabolism
  • Inflammatory Bowel Diseases* / therapy
  • Mesenchymal Stem Cell Transplantation
  • Mesenchymal Stem Cells* / immunology
  • Mesenchymal Stem Cells* / metabolism
  • Protein Processing, Post-Translational
  • Signal Transduction
  • Ubiquitination*

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was sponsored by the National Natural Science Fund of China (Grant no. 82250410378), 2022 Jiangsu Excellent postdoctoral program (Grant no. 2022ZB634), Zhenjiang key research and development plan (social development) (Grant no. SH2022062, SH2022091 and SH2023050) and Project of Suzhou Science and Technology (Grant no. SKY2022027).