ArticleExperimental and therapeutic medicine2021
MicroRNA-602 prevents the development of inflammatory bowel diseases in a microbiota-dependent manner.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Saikosaponin D Attenuates Postherpetic Neuralgia and Reduces Inflammation by Regulating Gut Microbiota in a Rodent Model.Biochemical genetics · 2026Article
- An overview of the role of the gut microbiota in rheumatoid arthritis.Microbiome research reports · 2026Review
- MicroRNAs as Key Modulators of Intestinal Barrier Function: Pattern Recognition Receptors, Epithelial Junctional Complexes, and Therapeutic Approaches.Digestive diseases and sciences · 2025Review
- The Role of microRNAs in Inflammatory Bowel Disease.International journal of molecular sciences · 2025Review
- The study on circRNA profiling uncovers the regulatory function of the hsa_circ_0059665/miR-602 pathway in breast cancer.Scientific reports · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
Inflammatory bowel diseases (IBD) are a group of chronic disorders occurring in the intestinal tract. Previous studies demonstrated that genetics and microbiota play critical roles in the pathogenesis of IBD. Discoveries of genes that may regulate the homeostasis of gut microbiota and pathogenesis of IBD have the potential to provide new therapeutic targets for IBD treatment. The results suggested that the expression level of microRNA (miR)-602 is negatively related to the development of IBD, and that miR-602 overexpression in mice may prevent inflammation and intestinal barrier injuries in dextran sulfate sodium (DSS)-induced IBD mice. It was also found that the microbiota is important for miR-602-mediated prevention of IBD, as the inhibitory effect of miR-602 was lost when the microbiota was depleted using antibiotics. Furthermore, co-housing or adoptive transfer of microbiota from miR-602 could attenuate the pathogenesis of IBD. In addition, it was demonstrated that miR-602 could target tumor necrosis factor receptor-associated factor 6 (TRAF6) in intestinal epithelial cells. Collectively, the present results suggest that miR-602 plays a protective role in DSS-induced IBD by targeting TRAF6 in a microbiota-dependent manner.
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