microRNA 192 (miR-192)

microRNA 192 (miR-192) is a short, endogenous, non-coding RNA molecule that regulates gene expression post-transcriptionally by binding to the 3′ untranslated region of mRNAs, causing mRNA degradation or inhibiting translation[1][3]. It is expressed in various human tissues, with notable roles in cell proliferation, differentiation, EMT, apoptosis, and fibrosis[1][2]. miR-192 is widely implicated in human disease, particularly in diabetic nephropathy, where its abnormal expression contributes to kidney fibrosis, and in various cancers, where it impacts cell cycle regulators (e.g., RB1)[1][2][4]. Its clinical relevance includes utility as a biomarker and as a potential therapeutic target; experimental drugs and interventions modulate miR-192 to affect disease progression in preclinical models[1][2]. miR-192’s extensive biological impact arises from its ability to regulate hundreds to thousands of target genes, reinforcing both its promise and challenges as a therapeutic target.

Other names

hsa-mir-192MIRN192MIR192miRNA192

Drugs modulate miR-192 expression (down-regulation or inhibition). Compounds affect pathways (e.g., TGF-β/Smad/miR-192) involved in fibrosis and cell proliferation.