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MicroRNA 1183 (miR-1183) is a member of the microRNA family, a class of small (about 22 nucleotides), evolutionarily conserved, non-coding RNA molecules that negatively regulate gene expression post-transcriptionally. Like other microRNAs, miR-1183 regulates gene expression by binding to complementary sequences in the 3′-untranslated region (3′-UTR) of target mRNAs—primarily leading to mRNA degradation or translational repression[1][4][5]. Its expression has been observed to be upregulated in several disease states, notably in rheumatic heart disease (RHD), pulmonary arterial hypertension (PAH) secondary to RHD, and in some cancers, such as locally advanced rectal cancer[2][4]. Mechanistically, predicted targets for miR-1183 include genes involved in cell signaling and proliferation such as CXCR4, EGF, and EGFR[2][4]. The disease-associated changes in miR-1183 levels suggest its potential as a non-invasive circulating disease biomarker, especially for cardiovascular and autoimmune disorders[2][4]. However, to date, miR-1183 itself is not established as a direct pharmacological target, nor are there drugs specifically developed to interact with it or modulate its function. There is no evidence of attendant safety concerns or therapeutic challenges specific to miR-1183, but as with other miRNAs, modulation for therapy presents challenges in specificity and delivery[1][5].
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