MicroRNA-762 (miR-762)

MicroRNA-762 (miR-762) is a small, endogenous non-coding RNA molecule that functions as a negative regulator of gene expression by binding messenger RNAs, typically resulting in translational repression or mRNA degradation[1][2]. Its actions are primarily post-transcriptional. miR-762 is implicated in diverse biological processes: - It regulates **mitochondrial function** and induces apoptosis in cardiomyocytes by targeting mitochondrial ND2, thus inhibiting ATP production, increasing ROS generation, impairing mitochondrial complex I activity, and promoting cell death under ischemia/reperfusion (I/R) injury conditions[1]. - In cancer, particularly **breast cancer**, miR-762 promotes cell proliferation and invasion by directly targeting and downregulating interferon regulatory factor 7 (IRF7)[2]. - It is upregulated in **systemic lupus erythematosus (SLE)** and **neuropsychiatric SLE (NPSLE)**, where it suppresses GIPC3 and may contribute to disease development[4]. - Other reported targets include IFITM5 in bone cells, linking miR-762 to bone mineralization, and genes like RNase7 and ST2 in epithelial responses to infection[1][2]. There are currently no approved drugs that specifically target miR-762, but its roles in disease make it a candidate therapeutic target for conditions such as myocardial infarction, certain cancers, and autoimmune diseases. Safety considerations include potential unintended effects due to widespread regulatory roles typical of microRNAs.

Other names

hsa-miR-762MIR762hsa-mir-762

Post-transcriptional gene silencing by binding target mRNA (inhibits translation or promotes degradation); Direct inhibition of mitochondrial ND2 translation in cardiomyocytes; Downregulation of IRF7 in breast cancer; Suppression of IFITM5 during bone mineralization; Suppression of GIPC3 in SLE/NPSLE