ArticleDrug design, development and therapy2015
Simvastatin prevents isoproterenol-induced cardiac hypertrophy through modulation of the JAK/STAT pathway.
Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 58 citations in OpenAlex.
- Geraniin attenuates isoproterenol-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Contributions of mechanical loading and hormonal changes to eccentric hypertrophy during volume overload: A Bayesian analysis using logic-based network models.PLoS computational biology · 2025Article
- Myrcene enhances the cardioprotective effect through matrix remodelling in an experimental model of heart failure.Archives of medical science : AMS · 2025Article
- Identification of biomarkers associated with energy metabolism in hypertrophic cardiomyopathy and exploration of potential mechanisms of roles.Frontiers in cardiovascular medicine · 2025Article
- Simvastatin Significantly Reduced Alcohol-Induced Cardiac Damage in Adolescent Mice.Cardiovascular toxicology · 2024Article
- Research progress on post-translational modification of proteins and cardiovascular diseases.Cell death discovery · 2023Review
- Huntington's disease phenotypes are improved via mTORC1 modulation by small molecule therapy.PloS one · 2022Article
- Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics.Disease markers · 2022Article
- Network Pharmacology andFrontiers in pharmacology · 2022Article
- Molecular Mechanisms of Hepatoblastoma.Seminars in liver disease · 2021Article
- Evaluation of Anti-hypertrophic Potential ofIndian journal of clinical biochemistry : IJCB · 2021Article
- Schisandrin Protects against Norepinephrine-Induced Myocardial Hypertrophic Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Farnesol attenuates oxidative stress and liver injury and modulates fatty acid synthase and acetyl-CoA carboxylase in high cholesterol-fed rats.Environmental science and pollution research international · 2020Article
- The peptide compound urantide regulates collagen metabolism in atherosclerotic rat hearts and inhibits the JAK2/STAT3 pathway.Molecular medicine reports · 2020Article
- Simvastatin nanoliposome induces myocardial and hepatic toxicities due to its absorption enhancement in mice.Asian journal of pharmaceutical sciences · 2020Article
- Comparative Study of the Therapeutic Potential of Mesenchymal Stem Cells Derived from Adipose Tissue and Bone Marrow on Acute Myocardial Infarction Model.Oman medical journal · 2019Article
- Mitochondrial protection by simvastatin against angiotensin II-mediated heart failure.British journal of pharmacology · 2019Article
- Protocatechuic aldehyde protects against isoproterenol-induced cardiac hypertrophy via inhibition of the JAK2/STAT3 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Effects of Cardiovascular Risk Factors on Cardiac STAT3.International journal of molecular sciences · 2018Review
- Protection of Luteolin-7-O-glucoside against apoptosis induced by hypoxia/reoxygenation through the MAPK pathways in H9c2 cells.Molecular medicine reports · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Simvastatin (SIM) is a lipid-soluble inhibitor of hydroxy-3-methylglutaryl coenzyme A reductase with multiple reported therapeutic benefits. The present study was designed to investigate the effect of pretreatment with SIM on isoproterenol (ISO)-induced cardiac hypertrophy in rats. Twenty-four male albino Wistar rats weighing 180-200 g were divided into four groups. Groups I and III received normal saline while groups II and IV received SIM (10 mg/kg body weight) for 30 days per gavage. In the last 7 days, rats of groups III and IV were administered ISO (5 mg/kg) intraperitoneally to induce cardiac hypertrophy. Administration of ISO induced an increase in heart-to-body weight (HW/BW) ratio, an increase in serum interleukin-6, and elevated systolic and diastolic blood pressure. Serum levels of lipids, cardiovascular risk indices, and cardiac troponin I and creatine phosphokinase-MB showed significant increase in ISO-induced hypertrophic rats. Histopathological examination of heart tissue revealed focal areas of subendocardium degeneration, mononuclear cellular infiltrations, fibrous tissue deposition, and increased thickness of the myocardium of left ventricle. In addition, ISO-administered rats exhibited significant upregulation of cardiac Janus kinase, phosphorylated signal transducer and activator of transcription, and nuclear factor-kappa B. Pretreatment with SIM significantly prevented ISO-induced cardiac hypertrophy, alleviated the altered biochemical parameters, and improved the heart architecture. In conclusion, our study provides evidence that SIM prevented the development of cardiac hypertrophy via modulation of the Janus kinase/signal transducer and activator of transcription-signaling pathway in the heart of ISO-administered animals.
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