ArticleMolecular therapy. Nucleic acids2019
A Chymase Inhibitory RNA Aptamer Improves Cardiac Function and Survival after Myocardial Infarction.
Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Beneficial Effects of Chymase Inhibition on Cardiac Diastolic Function and Remodeling Induced by Chronic Angiotensin II Stimulation.International journal of molecular sciences · 2025Article
- RNA aptamer-mediated RNA nanotechnology for potential treatment of cardiopulmonary diseases.Pharmacological research · 2025Review
- Pathophysiological Role of Chymase-Activated Matrix Metalloproteinase-9.Biomedicines · 2022Review
- Cardiac biomarkers and detection methods for myocardial infarction.Molecular & cellular toxicology · 2022Review
- Kinins and chymase: the forgotten components of the renin-angiotensin system and their implications in COVID-19 disease.American journal of physiology. Lung cellular and molecular physiology · 2021Review
- Mechanism of Albuminuria Reduction by Chymase Inhibition in Diabetic Mice.International journal of molecular sciences · 2020Article
- Current Perspectives on Aptamers as Diagnostic Tools and Therapeutic Agents.Pharmaceutics · 2020Review
- Is chymase 1 a therapeutic target in cardiovascular disease?Expert opinion on therapeutic targetsReview
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have reported that mast cell chymase, an angiotensin II-generating enzyme, is important in cardiovascular tissues. Recently, we developed a new chymase-specific inhibitory RNA aptamer, HA28, and we evaluated the effects of HA28 on cardiac function and the mortality rate after myocardial infarction. Echocardiographic parameters, such as the left ventricular ejection fraction, fractional shortening, and the ratio of early to late ventricular filling velocities, were significantly improved by treatment with HA28 after myocardial infarction. The mortality rate was significantly reduced in the HA28-treated group. Cardiac chymase activity and chymase gene expression were significantly higher in the vehicle-treated myocardial infarction group, and these were markedly suppressed in the HA28-treated myocardial infarction group. The present study provides the first evidence that a single-stranded RNA aptamer that is a chymase-specific inhibitor is very effective in the treatment of acute heart failure caused by myocardial infarction. Chymase may be a new therapeutic target in post-myocardial infarction pathophysiology.
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Registered trials
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