MicroRNA-223 target messenger RNAs (miR-223 targets)

MicroRNA-223 (miR-223) target messenger RNAs (mRNAs) represent a complex regulatory network primarily involved in the control of myeloid cell lineage commitment and the modulation of innate immune responses (Johnnidis et al., 2008, Nature). miR-223 is highly enriched in neutrophils and macrophages, where it functions as a critical rheostat for inflammation by binding to the 3' untranslated regions (UTRs) of specific mRNAs to induce their degradation or repress their translation (Haneklaus et al., 2013, FEBS Letters). One of its most significant targets is the NLRP3 inflammasome; by suppressing NLRP3, miR-223 limits the production of pro-inflammatory cytokines like IL-1β, thereby preventing excessive tissue damage during infection or injury (Bauernfeind et al., 2012, J Immunol). Other key targets include transcription factors such as MEF2C, which regulates the proliferation of myeloid progenitor cells, and E2F1 and STAT3, which are essential for cell cycle progression and survival (Pulikkan et al., 2010, Blood). Dysregulation of the miR-223/target axis is a hallmark of several diseases, including acute myeloid leukemia (AML), where miR-223 loss leads to the overexpression of oncogenic targets, and chronic inflammatory conditions like rheumatoid arthritis and inflammatory bowel disease (IBD) (Neudecker et al., 2017, JCI Insight). Therapeutic strategies currently under investigation include the use of miR-223 mimics to restore homeostatic control over inflammatory targets or antagomirs to modulate hematopoietic recovery in specific clinical contexts (Ye et al., 2018, Molecular Therapy).

Other names

miR-223 regulated geneshsa-miR-223-3p targetsMicroRNA-223-3p target transcriptsmiR-223-3p target mRNAs

MicroRNA-mediated post-transcriptional gene silencing via 3' UTR binding, leading to mRNA degradation or translational inhibition of target transcripts.