AI Article Synopsis

  • MicroRNAs (miRNAs) are small RNA molecules that regulate gene expression and impact over 30% of protein-coding genes, particularly in inflammatory processes and intestinal health.
  • Research indicates that dysregulated miRNA expression is closely linked to inflammatory bowel disease (IBD), specifically Crohn's disease and ulcerative colitis, highlighting their potential role as disease biomarkers.
  • Despite established regulatory functions of miRNAs in IBD, effective clinical biomarkers are still lacking, necessitating further research to leverage miRNAs for therapeutic approaches in personalized medicine.

Article Abstract

MicroRNAs (miRNAs), small non-coding RNAs composed of 18-24 nucleotides, are potent regulators of gene expression, contributing to the regulation of more than 30% of protein-coding genes. Considering that miRNAs are regulators of inflammatory pathways and the differentiation of intestinal epithelial cells, there is an interest in exploring their importance in inflammatory bowel disease (IBD). IBD is a chronic and multifactorial disease of the gastrointestinal tract; the main forms are Crohn's disease and ulcerative colitis. Several studies have investigated the dysregulated expression of miRNAs in IBD, demonstrating their important roles as regulators and potential biomarkers of this disease. This editorial presents what is known and what is expected regarding miRNAs in IBD. Although the important regulatory roles of miRNAs in IBD are clearly established, biomarkers for IBD that can be applied in clinical practice are lacking, emphasizing the importance of further studies. Discoveries regarding the influence of miRNAs on the inflammatory process and the exploration of their role in gene regulation are expected to provide a basis for the use of miRNAs not only as potent biomarkers in IBD but also as therapeutic targets for the control of inflammatory processes in personalized medicine.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11056918PMC
http://dx.doi.org/10.3748/wjg.v30.i16.2184DOI Listing

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