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MicroRNA-1 (miR-1) is a highly conserved, muscle-specific non-coding RNA that plays a critical role in the development and maintenance of cardiac and skeletal muscle (Zhao et al., 2005). It is one of the most abundant microRNAs in the heart and is essential for regulating cardiogenesis, conduction systems, and myogenic differentiation by targeting key transcription factors and signaling molecules like Hand2 and HDAC4 (Yang et al., 2007). In disease contexts, miR-1 is frequently downregulated in various cancers, where it acts as a tumor suppressor by inhibiting cell proliferation and migration (Nasser et al., 2008). Conversely, its dysregulation in the heart is linked to conditions such as myocardial infarction, cardiac hypertrophy, and arrhythmias, making it a significant biomarker for cardiac injury (Wang et al., 2010). Therapeutically, miR-1 is being explored through the use of mimics to restore its tumor-suppressive function or antagomirs to modulate its activity in cardiovascular pathologies (Karakas et al., 2017). However, clinical application faces hurdles related to precise delivery and the potential for off-target effects across its broad network of mRNA targets (Title et al., 2015).
MicroRNA-1 functions through the RNA-induced silencing complex (RISC) to bind to the 3' untranslated region (UTR) of target messenger RNAs (mRNAs), leading to translational inhibition or mRNA degradation (Bartel, 2004).
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