Myocardial infarction associated transcript (MIAT)

Myocardial infarction associated transcript (MIAT) is a long non-coding RNA (lncRNA) originally identified in studies of genetic risk for myocardial infarction and subsequently found to regulate key cellular processes including proliferation, apoptosis, and fibrosis through acting as a competing endogenous RNA (ceRNA). MIAT is nuclear-localized, functions as a molecular sponge for several microRNAs (e.g., miR-24, miR-22-3p, miR-150), and modulates gene expression involved in cardiovascular and neurological diseases as well as various cancers. Abnormal MIAT expression is observed in disease states such as cardiac fibrosis, myocardial hypertrophy, diabetic cardiomyopathy, schizophrenia, ischemic stroke, and solid tumors. Experimental knockdown of MIAT ameliorates cardiac dysfunction and fibrosis in animal models, indicating therapeutic potential. Clinically, MIAT RNA levels and sequence polymorphisms are being investigated as biomarkers for disease risk and severity. No approved drugs directly target MIAT, but RNA-based inhibition strategies are under study.

Other names

FLJ25967RNCR2GomafuNCRNA00066LINC00066lncRNA-MIATnon-protein coding RNA 66C22orf35GOMAFUMI related novel mRNAlong intergenic non-protein coding RNA 66retinal non-coding RNA 2

siRNA/antisense oligonucleotide: Inhibition of MIAT expression, leading to reduced cardiac fibrosis/apoptosis; CeRNA mechanism: MIAT acts as a microRNA sponge, regulating miRNA activity (e.g., miR-24, miR-150, miR-22-3p, miR-150-5p), which in turn modulates expression of target proteins such as Furin, TGF-β1, P300, DAPK2