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Beyond the paradox: Cardiac‐specific miR‐106a delivery as a translational turning point for heart failure?

Year: 2025
Type: article
Abstract: Heart failure (HF) remains a global health burden and a leading cause of death and disability.In Asia, HF prevalence is projected to reach 74.5 million by 2050, a 127.6% increase from 2025, 1 driven by rising cardiometabolic disease across the region.While current therapies target haemodynamic impairment and pathological neurohormonal hyperactivation, they offer limited benefit against progressive myocardial decline and cardiovascular mortality.Novel therapeutics are urgently needed to overcome challenges of poor tissue specificity, limited intracellular delivery and suboptimal pharmacokinetics.MicroRNAs (miRNAs) are small non-coding RNAs, typically 20-24 nucleotides long, that regulate key posttranscriptional gene expression by binding to complementary sequences in messenger RNAs (mRNAs), leading to mRNA degradation or inhibition of translation.MiR-NAs have recently emerged as promising biomarkers and potential therapeutic targets in HF.Their clinical translation, however, hinges on precise delivery to minimize off-target effects and enhancing biodistribution.In this context, Lu et al. recently reported a cardiac targeting peptide (CTP; 12-amino acid sequence APWHLSSQYSRT) conjugated to miR-106a (CTP-miR-106a), which reversed cardiac hypertrophy and dysfunction in an angiotensin II/isoproterenol-induced mouse model of HF. 2 This study builds on prior in vitro evidence demonstrating that
Language: English
Open Access status: gold
Estimated APC paid: $2,420
OpenAlex ID: W4414103790
FWCI:
Cites: 11
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Related to: 10