miR-574-5p in epigenetic regulation and Toll-like receptor signaling
miR-574-5p is an unusual microRNA (miRNA) that is often upregulated or downregulated following exposure to irradiation or toxic chemicals; bacterial, parasitic or viral infection; and a variety of other disease conditions. Canonically, miR-574-5p epigenetically regulates the expression of many messe...
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Published in | Cell communication and signaling Vol. 22; no. 1; p. 567 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
England
BioMed Central Ltd
26.11.2024
BioMed Central |
Subjects | |
Online Access | Get full text |
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Summary: | miR-574-5p is an unusual microRNA (miRNA) that is often upregulated or downregulated following exposure to irradiation or toxic chemicals; bacterial, parasitic or viral infection; and a variety of other disease conditions. Canonically, miR-574-5p epigenetically regulates the expression of many messenger RNAs (mRNAs) through miRNA-mediated posttranscriptional regulation, thereby affecting cellular physiology or pathophysiology and contributing to the pathogenesis or progression of a variety of diseases. However, recent studies have established that in addition to serving as a fine-tuning repressor of gene expression, miR-574-5p also stimulates gene expression as an endogenous ligand for Toll-like receptor-8/7 (TLR8/7). Indeed, the binding of miR-574-5p to TLR8/7 triggers the TLR signaling pathway, leading to the induction of interferons, inflammatory cytokines and autoimmune signaling. These findings suggest that miR-574-5p is not only an important epigenetic regulator of gene expression, but also an important regulator of immune and inflammatory responses. Abnormal miR-574-5p-TLR8/7 signaling has been shown to be tightly associated with inflammation-related cancers and a number of autoimmune disorders. miR-574-5p can serve as a potential biomarker for many diseases. Most importantly, miR-574-5p is a promising therapeutic target for the treatment or prevention of human disorders, especially infectious diseases, cancers and autoimmune diseases. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 1478-811X 1478-811X |
DOI: | 10.1186/s12964-024-01934-x |