ArticleBritish journal of pharmacology2014
Olmesartan prevents cardiac rupture in mice with myocardial infarction by modulating growth differentiation factor 15 and p53.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- GDF15 as a sentinel of metabolic integrity: a narrative review of stress signaling, multisystem pathophysiology, and therapeutic potential.Frontiers in endocrinology · 2026Review
- Proteomic analysis of plasma proteins from patients with cardiac rupture after acute myocardial infarction using TMT-based quantitative proteomics approach.Clinical proteomics · 2024Article
- Positive effect of Periostin on repair of Isopreternol induced ischemic damaged cardiomyocyte: an in vitro model.Regenerative therapy · 2022Article
- MicroRNA-122-5p Aggravates Angiotensin II-Mediated Myocardial Fibrosis and Dysfunction in Hypertensive Rats by Regulating the Elabela/Apelin-APJ and ACE2-GDF15-Porimin Signaling.Journal of cardiovascular translational research · 2022Article
- Cardioprotective effect of MLN4924 on ameliorating autophagic flux impairment in myocardial ischemia-reperfusion injury by Sirt1.Redox biology · 2021Article
- GDF15 and Cardiac Cells: Current Concepts and New Insights.International journal of molecular sciences · 2021Review
- Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779.Circulation · 2021Article
- [Contribution of sympathetic activation to antihypertrophic memory after regression of exercise-induced physiological myocardial hypertrophy in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- RAS inhibition in resident fibroblast biology.Cellular signalling · 2021Review
- Article
- Excessive fibroblast growth factor 23 promotes renal fibrosis in mice with type 2 cardiorenal syndrome.Aging · 2021Article
- A Modified Surgical Ventricular Reconstruction in Post-infarction Mice Persistently Alleviates Heart Failure and Improves Cardiac Regeneration.Frontiers in cardiovascular medicine · 2021Article
- Review
- Inhibition of Platelets by Clopidogrel Suppressed Ang II-Induced Vascular Inflammation, Oxidative Stress, and Remodeling.Journal of the American Heart Association · 2018Article
- Olmesartan attenuates pressure-overload- or post-infarction-induced cardiac remodeling in mice.Oncotarget · 2018Article
- Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3β/cyclin D1 signalling pathway.Cardiovascular research · 2017Article
- Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis.Scientific reports · 2016Article
- Effect of Atorvastatin on Growth Differentiation Factor-15 in Patients with Type 2 Diabetes Mellitus and Dyslipidemia.Diabetes & metabolism journal · 2016Article
- Genistein alleviates pressure overload-induced cardiac dysfunction and interstitial fibrosis in mice.British journal of pharmacology · 2015Article
- Effects of olmesartan on endothelial progenitor cell mobilization and function in carotid atherosclerosis.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeCardiac rupture is a catastrophic complication that occurs after acute myocardial infarction (MI) and, at present, there are no effective pharmacological strategies for preventing this condition. Here we investigated the effect of the angiotensin II receptor blocker olmesartan (Olm) on post-infarct cardiac rupture and its underlying mechanisms of action. EXPERIMENTAL APPROACH: C57Bl/6 mice with MI were treated with Olm, aldosterone (Aldo) or vehicle. Cultured neonatal cardiomyocytes and fibroblasts were exposed to normoxia or anoxia and treated with angiotensin II (Ang II), RNH6270 (active ingredient of Olm) or Aldo. KEY
resultsThe mortality rate and incidence of cardiac rupture in MI mice during the first week in the Olm-treated group were significantly lower than in the vehicle-treated group. Olm or RNH6270 reduced myeloperoxidase staining in the infarcted myocardium, decreased apoptosis in cultured cardiomyocytes and fibroblasts, as assessed by Hoechst staining and TUNEL assay, attenuated the accumulation of p53 and phosphorylated p53 and cleaved caspase 3 induced by MI or Ang II, as assessed by Western blotting, and up-regulated growth differentiation factor-15 (GDF-15). In cultured cardiomyocytes and fibroblasts, treatment with Ang II, Aldo or anoxia significantly down-regulated the expression of GDF-15. CONCLUSIONS AND IMPLICATIONS: Olm prevents cardiac rupture through inhibition of apoptosis and inflammation, which is attributable to the down-regulation of p53 activity and up-regulation of GDF-15. Our findings suggest that early administration of an AT1 receptor anatagonist to patients with acute MI is a potential preventive approach for cardiac rupture.
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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.