ArticleMolecular therapy : the journal of the American Society of Gene Therapy2017
The Efficacy of Cardiac Anti-miR-208a Therapy Is Stress Dependent.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Are RNA Therapies a Solid Foundation or a Frontier Yet to Be Conquered?International journal of molecular sciences · 2026Review
- MicroRNA, MicroRNA-lncRNA and MicroRNA-Circular RNA axes, and exosomal MicroRNAs: driving exercise-induced cardioprotection in heart failure.Frontiers in cell and developmental biology · 2026Review
- Hypoxia-responsive zinc finger E-box-binding homeobox 2 (ZEB2) regulates a network of calcium-handling genes in the injured heart.Cardiovascular research · 2024Article
- Non-Coding RNA-Targeted Therapy: A State-of-the-Art Review.International journal of molecular sciences · 2024Review
- The Role of miRNA in Renal Fibrosis Leading to Chronic Kidney Disease.Biomedicines · 2023Review
- Cardiac microRNAs: diagnostic and therapeutic potential.Archives of medical science : AMS · 2023Article
- MicroRNAs as therapeutic targets in cardiovascular disease.The Journal of clinical investigation · 2022Review
- miR-208a in Cardiac Hypertrophy and Remodeling.Frontiers in cardiovascular medicine · 2021Review
- MicroRNAs in Chronic Kidney Disease: Four Candidates for Clinical Application.International journal of molecular sciences · 2020Review
- Extracellular vesicular MicroRNA-27a* contributes to cardiac hypertrophy in chronic heart failure.Journal of molecular and cellular cardiology · 2020Article
- Effects of Oxidative Stress on Protein Translation: Implications for Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- Preclinical and Clinical Development of Noncoding RNA Therapeutics for Cardiovascular Disease.Circulation research · 2020Review
- miR-15a/-16 Inhibit Angiogenesis by Targeting the Tie2 Coding Sequence: Therapeutic Potential of a miR-15a/16 Decoy System in Limb Ischemia.Molecular therapy. Nucleic acids · 2019Article
- MicroRNA-221 Is Cardioprotective and Anti-fibrotic in a Rat Model of Myocardial Infarction.Molecular therapy. Nucleic acids · 2019Article
- Noncoding RNAs regulating cardiac muscle mass.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Review
- Immune Regulation of Tissue Repair and Regeneration via miRNAs-New Therapeutic Target.Frontiers in bioengineering and biotechnology · 2018Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are important regulators of biology and disease. Recent animal efficacy studies validate the therapeutic benefit of miRNA modulation and underscore the therapeutic value of miRNA-targeting oligonucleotides. However, whether disease conditions (stress) influence the pharmacological effects of an anti-miR is currently unknown. To study the effect of disease on target regulation after anti-miR treatment, we injected animals with anti-miR-208a, a synthetic oligonucleotide that inhibits the cardiomyocyte-specific miR-208a. Our data indicate that the presence of stress increases the number of regulated miR-208a targets, and that higher stress levels correlate with stronger target derepression. Additionally, the type of stress also influences which targets are regulated upon miR-208a inhibition. Studies in a large animal model indicate a similar stress-dependent anti-miR effect. Subsequent in vitro studies suggest that the influence of stress on anti-miR efficacy depends at least in part on increased cellular anti-miR uptake. These data indicate that the pharmacological effect of anti-miRs is stronger under disease conditions, and that both the type and severity of disease determine the therapeutic outcome. These facts will be important for assessing the therapeutic dose and predicting the therapeutic outcome when applying anti-miRs in a clinical setting.
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