ArticleMolecular medicine reports2022
Schisandrin A protects against isoproterenol‑induced chronic heart failure via miR‑155.
Article in Molecular medicine reports, 2022. 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, 18 citations in OpenAlex.
- The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026Review
- Targeted Delivery of Schisandrin A to Cardiac Endothelium Alleviates Myocardial Ischemia-Reperfusion Injury via Suppression of Ferroptosis.International journal of nanomedicine · 2026Article
- Interpretation of the molecular mechanism and therapeutic potential of microRNA‑155 in cardiovascular and cerebrovascular diseases (Review).International journal of molecular medicine · 2026Review
- Targeting miR-144-5p/ACSM1 Axis Alleviates Doxorubicin-Induced Heart Failure by Inhibiting Lipid Peroxidation.Current medical science · 2025Article
- Review
- A comparison of urinary bladder weight in male and female mice across five models of diabetes and obesity.Frontiers in pharmacology · 2023Article
- Effect of injection of different doses of isoproterenol on the hearts of mice.BMC cardiovascular disorders · 2022Article
- Review
- Non-coding RNAs in necroptosis, pyroptosis, and ferroptosis in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schisandrin A (Sch A) has a protective effect on cardiomyocytes. Circulating miR‑155 levels are related to chronic heart failure (CHF). The present study aimed to clarify the role and the molecular mechanism of Sch A in CHF. C57BL/6JGpt mice were used for an isoproterenol (ISO)‑induced CHF model to collect heart samples. Echocardiography was employed to detect heartbeat indicators. The degree of myocardial hypertrophy was evaluated based on the measurement of heart weight (HW), body weight (BW) and tibia length (TL) and the observation using hematoxylin‑eosin staining. Sprague‑Dawley rats were purchased for the separation of neonatal rat ventricular myocytes (NRVMs), which were treated with ISO for 24 h. Transfection regulated the level of miR‑155. The viability of NRVMs was detected via MTT assay. The mRNA and protein levels were measured via reverse transcription‑quantitative PCR and western blotting and immunofluorescence was used to detect the content of α‑smooth muscle actin (α‑SMA). Treatment with ISO resulted in rising left ventricular posterior wall thickness, intra‑ventricular septum diastole, left ventricular end diastolic diameter, left ventricular end systolic diameter, HW/BW, HW/TL and falling ejection fraction and fractional shortening, the trend of which could be reversed by Sch A. Sch A ameliorated myocardial hypertrophy in CHF mice. In addition, Sch A inhibited ISO‑induced upregulated expressions of atrial natriuretic peptide, B‑type natriuretic peptide, B‑myosin heavy chain and miR‑155 in myocardial tissue. Based on the results
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