ArticleCardiovascular toxicology2022
Rosuvastatin Alleviates Coronary Microembolization-Induced Cardiac Injury by Suppressing Nox2-Induced ROS Overproduction and Myocardial Apoptosis.
Article in Cardiovascular toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Possible protective effect of rosuvastatin in chemotherapy-induced cardiotoxicity in HER2 positive breast cancer patients: a randomized controlled trial.Medical oncology (Northwood, London, England) · 2024Trial
- Role of NADPH oxidase 2-derived reactive oxygen species in cardiac electrophysiological disorders.Channels (Austin, Tex.) · 2026Review
- Research Progress of Regulatory Cell Death in Coronary Microembolization.International journal of medical sciences · 2025Review
- Review
- The Possible Role of Rosuvastatin Therapy in HFpEF Patients-A Preliminary Report.Diagnostics (Basel, Switzerland) · 2024Article
- Gastrodin Alleviates Angiotensin II-Induced Hypertension and Myocardial Apoptosis via Inhibition of the PRDX2/p53 Pathway In Vivo and In Vitro.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Structure, Activation, and Regulation of NOX2: At the Crossroad between the Innate Immunity and Oxidative Stress-Mediated Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- The effect of lipid-lowering therapies on the pro-inflammatory and anti-inflammatory properties of vascular endothelial cells.PloS one · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
To explore the mechanism by which rosuvastatin prevents coronary microembolism (CME)-induced cardiac injury and cardiomyocyte apoptosis. Animal and cell models of CME were established and treated with different doses of rosuvastatin. Echocardiography and histological staining were applied to assess left ventricular function and cardiac injury. Masson trichrome staining was used to evaluate fibrin deposition in the myocardium. The activity of lactate dehydrogenase (LDH) in serum and cell culture supernatant was detected. TUNEL staining and flow cytometry were used to evaluate apoptosis in myocardium and cardiomyocytes, respectively. The activity of ROS was revealed by DHE staining. The expression levels of Nox2, cleaved caspase-3, cytochrome C, p53, Bax and Bcl-2 were also detected. Rosuvastatin pretreatment improved the left ventricular function of CME mice and reduced inflammatory cell infiltration and fibrin deposition in the myocardium. Rosuvastatin reduced the production of ROS by inhibiting the expression of Nox2. Rosuvastatin also downregulated pro-apoptotic proteins cleaved caspase-3, cytochrome C, p53 and Bax, and upregulated anti-apoptotic Bcl-2. Rosuvastatin mitigates CME-induced cardiac injury by inhibiting Nox2-induced ROS overproduction and alleviating p53/Bax/Bcl-2-dependent cardiomyocyte apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.