ArticleMolecular medicine reports2018
Rosuvastatin relieves myocardial ischemia/reperfusion injury by upregulating PPAR‑γ and UCP2.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Pooled it
- Cardiomyopeptide-Regulated PPARγ Expression Plays a Critical Role in Maintaining Mitochondrial Integrity and Preventing Cardiac Ischemia/Reperfusion Injury.International journal of medical sciences · 2025Article
- Sex difference in human diseases: mechanistic insights and clinical implications.Signal transduction and targeted therapy · 2024Review
- Rosuvastatin alleviated the liver ischemia reperfusion injury by activating the expression of peroxisome proliferator-activated receptor gamma (PPARγ).Journal of bioenergetics and biomembranes · 2021Article
- PPARγ in Ischemia-Reperfusion Injury: Overview of the Biology and Therapy.Frontiers in pharmacology · 2021Review
- Attenuation of the Na/K‑ATPase/Src/ROS amplification signaling pathway by astaxanthin ameliorates myocardial cell oxidative stress injury.Molecular medicine reports · 2020Article
- Rosuvastatin protects isolated hearts against ischemia-reperfusion injury: role of Akt-GSK-3β, metabolic environment, and mitochondrial permeability transition pore.Journal of physiology and biochemistry · 2020Article
- Rosuvastatin Alleviates Intestinal Injury by Down-Regulating the CD40 Pathway in the Intestines of Rats Following Traumatic Brain Injury.Frontiers in neurology · 2020Article
- Functional Implications of HMG-CoA Reductase Inhibition on Glucose Metabolism.Korean circulation journal · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate whether pretreatment with rosuvastatin (RS) can provide cardioprotection in a myocardial ischemia/reperfusion (MI/R) model. The protective effect of RS on myocardial oxygen‑glucose deprivation/reperfusion (OGD/R) injury was also evaluated by upregulating peroxisome proliferator‑activated receptor‑γ (PPAR‑γ). In the present study, MI/R model was established and activities of superoxide dismutase (SOD), lactate dehydrogenase (LDH), creatine kinase‑muscle/brain (CK‑MB), malondialdehyde (MDA), and troponin I/T were measured. The infarct size was measured using Evans blue staining and cell viability was measured by MTT assay. Reactive oxygen species (ROS) levels were assessed by flow cytometry. Caspase‑9, cytochrome c (cyt c), mitochondrial uncoupling protein 2 (UCP2) and PPAR‑γ expression levels were detected by reverse transcription‑quantitative polymerase chain reaction and western blotting. The results indicated that RS increased SOD activity, and decreased LDH, CK‑MB, MDA and troponin I/T activities. The effect of RS was reversed by atractyloside (ATR). RS inhibited myocardial infarct size, downregulated expression of caspase‑9 and cyt c and upregulated expression of UCP2 and PPAR‑γ by inhibiting ATR. Furthermore, the results indicated that RS promoted cardiomyocyte viability, inhibited LDH release, reduced ROS production, decreased expression of caspase‑9 and cyt c, and increased expression of UCP2 and PPAR‑γ following OGD/R damage. Therefore, the present study demonstrated that RS protects primary myocardial cells against OGD/R injury by regulating PPAR‑γ and UCP2. RS may be a promising therapeutic agent for treatment of MI/R injury.
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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 Socratic graph.