ArticleExperimental and therapeutic medicine2020
MicroRNA-155 promotes apoptosis of colonic smooth muscle cells and aggravates colonic dysmotility by targeting IGF-1.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Intertwined roles of microRNA-155 and metformin in osteoarthritis: Novel potential diagnostic, prognostic, and therapeutic modulators.World journal of orthopedics · 2025Review
- Selected microRNA Expression and Protein Regulator Secretion by Adipose Tissue-Derived Mesenchymal Stem Cells and Metabolic Syndrome.International journal of molecular sciences · 2024Article
- Exosomal microRNAs in cancer-related sarcopenia: Tumor-derived exosomal microRNAs in muscle atrophy.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colonic dysmotility as a complication of diabetes affects public health; however, the underlying molecular mechanisms have remained elusive. Insulin-like growth factor-1 (IGF-1) was previously demonstrated to prevent apoptosis of colonic smooth muscle cells (SMCs) and alleviate colonic dysmotility in diabetic rats. However, the regulatory mechanisms upstream of IGF-1 in colonic dysmotility have remained to be determined. The present study reports on microRNA-155 (miR-155), initially identified using bioinformatics, as a direct upstream regulator of IGF-1. In colonic SMCs, miR-155 negatively regulated IGF-1 expression at the post-transcriptional level, as identified through ectopic overexpression and knockdown experiments. A luciferase reporter assay further demonstrated that miR-155 inhibits IGF-1 through binding to its 3'-untranslated region. Furthermore, overexpression of miR-155 led to increased apoptosis of colonic SMCs and a decrease in the thickness of colonic smooth muscle tissues of diabetic mice, indicating miR-155 aggravates colonic dysmotility. By contrast, knockdown of miR-155 induced the opposite effect. Overall, the results of the present study suggest a role of miR-155 in colonic dysmotility, thereby providing a novel therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.