ReviewCardiovascular research2009
Eicosanoid signalling pathways in the heart.
Review in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
75 citing papers in PubMed, 181 citations in OpenAlex.
- Metabolic syndrome and a broken heart: trust your gut or risk your heart.American journal of physiology. Heart and circulatory physiology · 2026Review
- Aryl hydrocarbon receptor ligand 6-formylindolo[3,2-b]carbazole attenuates pressure overload cardiac hypertrophy by activating the CYP1A1/19(S)-hydroxyeicosatetraenoic acid (HETE) and suppressing midchain-HETEs/G protein coupled receptor 31 pathways.Drug metabolism and disposition: the biological fate of chemicals · 2026Article
- Revisiting Bill Lands' Hypotheses: HUFA Balance, Immuno-Metabolic Regulation, and Conflicting Clinical Evidence.Nutrients · 2026Review
- Sex-dependent alterations in cardiac cytochrome P450-mediated arachidonic acid metabolism in pressure overload-induced cardiac hypertrophy in rats.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- Arachidonic acid in aging: New roles for old players.Journal of advanced research · 2025Review
- Robust machine-learning based prognostic index using fatty acid metabolism genes predicts prognosis and therapy responses in glioblastoma.Journal of Cancer · 2025Article
- Sini decoction alleviates inflammation injury after myocardial infarction through regulating arachidonic acid metabolism.Chinese herbal medicines · 2025Article
- Metabolomics in Atrial Fibrillation: Unlocking Novel Biomarkers and Pathways for Diagnosis, Prognosis, and Personalized Treatment.Journal of clinical medicine · 2024Review
- The Altered Lipid Composition and Key Lipid Metabolic Enzymes in Thiacloprid-ResistantInternational journal of molecular sciences · 2024Article
- Impact of Reperfusion on Plasma Oxylipins in ST-Segment Elevation Myocardial Infarction.Metabolites · 2023Article
- Eicosanoid and eicosanoid-related inflammatory mediators and exercise intolerance in heart failure with preserved ejection fraction.Nature communications · 2023Article
- Sexual Dimorphism of the Mouse Plasma Metabolome Is Associated with Phenotypes of 30 Gene Knockout Lines.Metabolites · 2023Article
- The PNPLA family of enzymes: characterisation and biological role.Arhiv za higijenu rada i toksikologiju · 2023Article
- The association between eicosanoids and incident atrial fibrillation in the Framingham Heart Study.Scientific reports · 2022Article
- Quantitative Proteomics Analysis Reveals That Cyclooxygenase-2 Modulates Mitochondrial Respiratory Chain Complex IV in Cardiomyocytes.International journal of molecular sciences · 2022Article
- Article
- CYP450 Epoxygenase Metabolites, Epoxyeicosatrienoic Acids, as Novel Anti-Inflammatory Mediators.Molecules (Basel, Switzerland) · 2022Review
- Hyperhomocysteinemia dysregulates plasma levels of polyunsaturated fatty acids-derived eicosanoids.Life research · 2022Article
- Article
- Cardiac immune cell infiltration associates with abnormal lipid metabolism.Frontiers in cardiovascular medicine · 2022Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial phospholipids serve as primary reservoirs of arachidonic acid (AA), which is liberated through the rate-determining hydrolytic action of cardiac phospholipases A2 (PLA2s). A predominant PLA2 in myocardium is calcium-independent phospholipase A2beta (iPLA2beta), which, through its calmodulin (CaM) and ATP-binding domains, is regulated by alterations in local cellular Ca2+ concentrations and cardiac bioenergetic status, respectively. Importantly, iPLA2beta has been demonstrated to be activated by ischaemia through elevation of the concentration of myocardial fatty acyl-CoA, which abrogates Ca2+/CaM-mediated inhibition of iPLA2beta. AA released by PLA2-catalysed hydrolysis of phospholipids serves as a precursor for eicosanoids generated by pathways dependent on cyclooxygenases (COX), lipoxygenases (LOX), and cytochromes P450 (CYP). Eicosanoids initiate and propagate diverse signalling cascades, primarily through their interaction with cellular receptors and ion channels. However, during pathologic states such as ischaemia or congestive heart failure, eicosanoids contribute to multiple maladaptive changes including inflammation, alterations of cellular growth programmes, and activation of multiple transcriptional events leading to the deleterious sequelae of these pathologic states. This review summarizes the central roles of myocardial PLA(2)s in eicosanoid signalling in the heart, the major COX, LOX, and CYP pathways of eicosanoid generation in the myocardium, and the effects of important eicosanoids on receptor-, ion channel-, and transcription-mediated processes that facilitate cardiac hypertrophy, mediate ischaemic preconditioning, and precipitate arrhythmogenesis in response to pathologic stimuli.
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What OpenQuestion holds
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.