Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (694 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A class of compounds named after and generally derived from C20 fatty acids (eicosanoic acids) that includes prostaglandins; leukotrienes; thromboxanes, and hydroxyeicosatetraenoic acids. They have hormone-like effects mediated by specialized receptors (receptors, eicosanoid).
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Icosanoid; Eicosanoid; Icosanoids.
Where it fits in the MeSH classification
- Broader topics
- Fatty Acids, Unsaturated; Autacoids
- Narrower topics
- 5,8,11,14-Eicosatetraynoic Acid; 8,11,14-Eicosatrienoic Acid; Arachidonic Acids; Eicosapentaenoic Acid; Lipoxins; Prostaglandins; Leukotrienes
- See also
- Receptors, Eicosanoid
Related concepts
- Eicosanoic Acids
- Prostaglandins
- Leukotrienes
- Thromboxanes
- Hydroxyeicosatetraenoic Acids
- Receptors
- Eicosanoid
Research landscape
PubMed indexes 157,202 records tagged with the MeSH heading “Eicosanoids” (counts retrieved 2026-10-31). 11,138 of them (7.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 86,935 records.
Reviews account for 15,367 records (9.8%) and meta-analyses for 587. Randomized controlled trials number 7,278 (4.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 86,935 |
| 2000-2009 | 32,417 |
| 2010-2019 | 26,712 |
| 2020 onward | 11,138 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 15,367 | 9.8% |
| Meta-analyses | 587 | 0.4% |
| Randomized controlled trials | 7,278 | 4.6% |
Method: PubMed query "Eicosanoids"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
N-3 Fatty Acids (EPA and DHA) and Cardiovascular Health - Updated Review of Mechanisms and Clinical Outcomes [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Purpose of reviewWe synthesize the latest evidence (published 2020 to 2025) on the role of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in cardiovascular health, emphasizing biological mechanisms and key findings from observational studies and clinical trials related to cardiovascular disease (CVD) risk and outcomes.
- Closing excerpt
- Moderate intake appears safe and protective, while high dose EPA may offer added benefits in high-risk individuals but also might increase AF risk.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (164 words)
Purpose of reviewWe synthesize the latest evidence (published 2020 to 2025) on the role of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in cardiovascular health, emphasizing biological mechanisms and key findings from observational studies and clinical trials related to cardiovascular disease (CVD) risk and outcomes.Recent findingsEPA and DHA modulate lipid metabolism, inflammation, platelet and endothelial function, the gut-heart axis, ion channels and autonomic function via vagal tone, supporting cardiovascular health. While individual RCTs have produced variable results, updated cohort data and recent meta-analyses consistently link higher intake or circulating levels of EPA and DHA to reduced risk of cardiovascular events. However, evidence from RCTs indicates that high-dose supplementation may be associated with an increase in atrial fibrillation (AF) risk. Evidence supports a role for EPA and DHA in CVD prevention and treatment, with effects influenced by dose, formulation, and individual variability. Moderate intake appears safe and protective, while high dose EPA may offer added benefits in high-risk individuals but also might increase AF risk.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41247613 · DOI · PMC12628397
Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Anaphylaxis is a life-threatening complication of food allergen exposure.
- Closing excerpt
- Mice genetically deficient in cysteinyl leukotriene synthesis, or those treated with the arachidonate 5-lipoxygenase (aLOX5) antagonist zileuton, were protected from oral antigen-induced responses, whereas those elicited by intravenous injection were unaltered.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (131 words)
Anaphylaxis is a life-threatening complication of food allergen exposure. Although mechanisms governing anaphylaxis after intravenous injection are defined in mice, these models neglect mucosal exposure that accompanies ingestion. We investigated the role of mast cells within the intestine of mice and found that oral anaphylaxis required immunoglobulin E-Fcε receptor 1 (IgE-FcεR1) signaling. Intestinal mast cells were a heterogeneous population, shaped by epithelial cues. Compared with connective tissue mast cells found throughout the body, intestinal mast cells largely resided in the epithelium, displayed divergent transcriptomes and effector functions, and had a diminished ability to generate histamine, but they enhanced leukotriene synthesis. Mice genetically deficient in cysteinyl leukotriene synthesis, or those treated with the arachidonate 5-lipoxygenase (aLOX5) antagonist zileuton, were protected from oral antigen-induced responses, whereas those elicited by intravenous injection were unaltered.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40773543 · DOI · PMC12513082
Contribution of Prostaglandin E2-Induced Neuronal Excitation to Drug Resistance in Glioblastoma Countered by a Novel Blood-Brain Barrier Crossing Celecoxib Derivative [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Glioblastoma (GBM) is a highly aggressive brain tumor.
- Closing excerpt
- These findings underscore PGE2-induced neuronal excitation as a critical driver of drug resistance in GBM, and implicate compound 11 as a promising therapeutic agent to counteract PGE2-driven tumor recurrence.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
Glioblastoma (GBM) is a highly aggressive brain tumor. Its poor prognosis is primarily due to recurrence and resistance to standard therapies, such as temozolomide (TMZ). Emerging evidence suggests that neuronal excitation within the tumor microenvironment contributes to the progression and chemoresistance of GBM. This study identifies prostaglandin E2 (PGE2) as a key regulator of neuronal activity that promotes tumor resistance. It is demonstrated that PGE2 activates neurons via the prostaglandin E1 (EP1) receptor, leading to intracellular calcium influx and phosphorylation of calcium/calmodulin dependent protein kinase II (CaMKII), which enhances synaptic plasticity. Neuronal excitation results in upregulation of synaptic proteins and neurotransmitter alterations, notably increasing glutamine and asparagine levels, which correlate with heightened chemoresistance. Co-culture experiments confirmed that PGE2-stimulated neurons induce resistance in adjacent GBM cells, highlighting a neuron-tumor interaction that facilitates recurrence. To overcome this resistance mechanism, compound 11 is developed, a novel blood-brain barrier (BBB)-permeable celecoxib derivative that effectively inhibits PGE2 signaling. Treatment with compound 11 significantly reduces GBM growth, impairs neuronal excitation, and improves survival outcomes in preclinical models. These findings underscore PGE2-induced neuronal excitation as a critical driver of drug resistance in GBM, and implicate compound 11 as a promising therapeutic agent to counteract PGE2-driven tumor recurrence.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40658067 · DOI · PMC12520548
12-HETE is an Endogenous Modulator of BLT2 Triggering Vascular Degeneration, Dissection, and Rupture [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Thoracic aortic dissection (TAD), a life-threatening vascular emergency requiring urgent pharmacological intervention, prompted investigation into arachidonic acid metabolites based on their established roles in inflammation and vascular homeostasis.
- Closing excerpt
- These findings establish the 12-HETE-BLT2 axis as a key driver of TAD pathogenesis and validate its potential as a promising therapeutic target for clinical intervention.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Thoracic aortic dissection (TAD), a life-threatening vascular emergency requiring urgent pharmacological intervention, prompted investigation into arachidonic acid metabolites based on their established roles in inflammation and vascular homeostasis. Through comprehensive plasma metabolomics analysis performed in both TAD patients and a β-aminopropionitrile monofumarate (BAPN)-induced mouse model, significant elevation of 12-hydroxyeicosatetraenoic acid (12-HETE) was identified, accompanied by marked upregulation of its synthetic enzyme 12/15-lipoxygenase (12/15-LOX) in dissected aortic tissues. The pathogenetic significance was further demonstrated by the substantial protection against TAD progression that was observed in Alox15-deficient mice. Mechanistically, 12-HETE was confirmed to function as an endogenous ligand for the BLT2 receptor on macrophages, leading to activation of the NOX-1/ROS/NF-κB signaling cascade. This signaling activation was shown to induce inflammatory cytokine release and promote inflammatory cell recruitment, ultimately resulting in pathological phenotype switching of vascular smooth muscle cells. The therapeutic potential was validated by significant reduction in dissection rupture rates that was achieved with either the 12/15-LOX inhibitor ML351 or the BLT2 antagonist LY255283, with maximal efficacy being demonstrated when both agents were administered in combination. These findings establish the 12-HETE-BLT2 axis as a key driver of TAD pathogenesis and validate its potential as a promising therapeutic target for clinical intervention.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41194414 · DOI · PMC12849872
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Is depression associated with increased oxidative stress? A systematic review and meta-analysis [5]
- Research article Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality [6]
- Research article Omega-3 fatty acid supplementation for the treatment of children with attention-deficit/hyperactivity disorder symptomatology: systematic review and meta-analysis [7]
- Research article Effects of eicosapentaenoic acid versus docosahexaenoic acid on serum lipids: a systematic review and meta-analysis [8]
- Research article Meta-analysis and meta-regression of omega-3 polyunsaturated fatty acid supplementation for major depressive disorder [9]
- Research article A meta-analysis of trials of pulmonary hypertension: a clinical condition looking for drugs and research methodology [10]
References
- Djuricic I, Calder PC. N-3 Fatty Acids (EPA and DHA) and Cardiovascular Health - Updated Review of Mechanisms and Clinical Outcomes. . 2025. PMID 41247613 · DOI · PMC12628397
- Bachtel ND, Cullen JL, Liu M, Erickson SA, Kutyavin VI, El-Naccache DW, et al.. Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens. . 2025. PMID 40773543 · DOI · PMC12513082
- Shen CJ, Chen HC, Lin CL, Thakur A, Onuku R, Chen IC, et al.. Contribution of Prostaglandin E2-Induced Neuronal Excitation to Drug Resistance in Glioblastoma Countered by a Novel Blood-Brain Barrier Crossing Celecoxib Derivative. . 2025. PMID 40658067 · DOI · PMC12520548
- Li Y, Yu J, Chen W, Wang X, Tan X, Cui J, et al.. 12-HETE is an Endogenous Modulator of BLT2 Triggering Vascular Degeneration, Dissection, and Rupture. . 2026. PMID 41194414 · DOI · PMC12849872
- Black CN, Bot M, Scheffer PG, Cuijpers P, Penninx BW. Is depression associated with increased oxidative stress? A systematic review and meta-analysis. Psychoneuroendocrinology. 2015. PMID 25462890 · DOI
- Marklund M, Wu JHY, Imamura F, Del Gobbo LC, Fretts A, de Goede J, et al.. Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality. Circulation. 2019. PMID 30971107 · DOI · PMC6582360
- Bloch MH, Qawasmi A. Omega-3 fatty acid supplementation for the treatment of children with attention-deficit/hyperactivity disorder symptomatology: systematic review and meta-analysis. J Am Acad Child Adolesc Psychiatry. 2011. PMID 21961774 · DOI · PMC3625948
- Wei MY, Jacobson TA. Effects of eicosapentaenoic acid versus docosahexaenoic acid on serum lipids: a systematic review and meta-analysis. Curr Atheroscler Rep. 2011. PMID 21975919 · DOI
- Mocking RJ, Harmsen I, Assies J, Koeter MW, Ruhé HG, Schene AH. Meta-analysis and meta-regression of omega-3 polyunsaturated fatty acid supplementation for major depressive disorder. Transl Psychiatry. 2016. PMID 26978738 · DOI · PMC4872453
- Macchia A, Marchioli R, Marfisi R, Scarano M, Levantesi G, Tavazzi L, et al.. A meta-analysis of trials of pulmonary hypertension: a clinical condition looking for drugs and research methodology. Am Heart J. 2007. PMID 17540207 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.