ArticleCardiovascular research2012
Cardiac-generated prostanoids mediate cardiac myocyte apoptosis after myocardial ischaemia.
Article in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- The potential molecular mechanism underlying gypenoside amelioration of atherosclerosis in ApoEHeliyon · 2024Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Potential mechanisms underlying podophyllotoxin-induced cardiotoxicity in male rats: toxicological evidence chain (TEC) concept.Frontiers in pharmacology · 2024Article
- MiRNA-615-3p Alleviates Oxidative Stress Injury of Human Cardiomyocytes Via PI3K/Akt Signaling by Targeting MEF2A.Anatolian journal of cardiology · 2022Article
- Modulation of Prostanoids Profile and Counter-Regulation of SDF-1α/CXCR4 and VIP/VPAC2 Expression by Sitagliptin in Non-Diabetic Rat Model of Hepatic Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Article
- Effects of Shenfu Qiangxin Drink on HExperimental and therapeutic medicine · 2021Article
- Long non‑coding RNA MEG3 knockdown alleviates hypoxia‑induced injury in rat cardiomyocytes via the miR‑325‑3p/TRPV4 axis.Molecular medicine reports · 2021Article
- Cellular and Molecular Mechanism of Traditional Chinese Medicine on Ventricular Remodeling.Frontiers in cardiovascular medicine · 2021Review
- Innovative Approaches to Assess Intermediate Cardiovascular Risk Subjects: A Review From Clinical to Metabolomics Strategies.Frontiers in cardiovascular medicine · 2021Review
- miR-370 inhibits the oxidative stress and apoptosis of cardiac myocytes induced by hydrogen peroxide by targeting FOXO1.Experimental and therapeutic medicine · 2019Article
- CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain.EMBO molecular medicine · 2018Article
- Peroxisome proliferator-activated receptor γ is essential for secretion of ANP induced by prostaglandin DThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- Calcineurin signaling in the heart: The importance of time and place.Journal of molecular and cellular cardiology · 2017Review
- Positron emission tomography imaging of cardiomyocyte apoptosis with a novel molecule probe [18F]FP-DPAZn2.Oncotarget · 2015Article
- Mechanism of QSYQ on anti-apoptosis mediated by different subtypes of cyclooxygenase in AMI induced heart failure rats.BMC complementary and alternative medicine · 2015Article
- Multiobjective triclustering of time-series transcriptome data reveals key genes of biological processes.BMC bioinformatics · 2015Article
- 15-deoxy-Δ¹²,¹⁴-PGJ₂ promotes inflammation and apoptosis in cardiomyocytes via the DP2/MAPK/TNFα axis.International journal of cardiology · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsThe objective of the present study is to elucidate the pathogenic role of eicosanoids in myocardial infarction (MI). The accumulation of eicosanoid metabolites in ischaemic myocardium has been demonstrated in animal models and patients with MI, and it occurs in parallel with the development of irreversible cardiac damage. However, the key question that remains unanswered is whether cardiac-generated eicosanoids are the cause or the consequence of cardiac cell damage in MI. METHODS AND
resultsWe used a clinically relevant animal model of MI and metabolic profiling to monitor the eicosanoid profile in ischaemic myocardium. We demonstrate that ischaemia induces the generation of prostanoids mainly through the cyclooxygenase (COX)-1 pathway in the myocardium. Cardiac-generated prostanoids, particularly prostaglandin D(2) (PGD(2)), can directly induce apoptosis in cardiac myocytes. This effect involves the up-regulation of the pro-apoptotic gene, Fas ligand (FasL), in a D-type prostanoid receptor-independent manner. The treatment of the MI mice with low-dose aspirin effectively inhibits the ischaemia-induced prostanoid generation and FasL expression in the myocardium, leading to the reduction in cardiac apoptosis following cardiac ischaemia.
conclusionsCardiac ischaemia results in COX-1-mediated generation of prostanoids, which by inducing cardiac myocyte apoptosis, contribute to the cardiac cell loss following MI. The benefits of low-dose aspirin treatment in MI may be attributable, in part, to the inhibition of cardiac prostanoid generation and attenuation of apoptosis. Further understanding of the mechanisms underlying prostanoid-induced cardiac apoptosis may be of significant value in designing new therapeutic strategies to prevent aberrant cell loss following MI and subsequent progression to heart failure.
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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.