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 (697 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
An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.
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: (all-Z)-5,8,11,14-Eicosatetraenoic acid; Vitamin F; Arachidonic Acid, Sodium Salt; Sodium Arachidonate; Arachidonate, Sodium; Arachidonic Acid, Cesium Salt, (all-Z)-Isomer; Arachidonic Acid, Cerium Salt, (all-Z)-Isomer; Arachidonic Acid, Potassium Salt, (all-Z)-Isomer.
Where it fits in the MeSH classification
- Broader topics
- Arachidonic Acids
Research landscape
PubMed indexes 19,936 records tagged with the MeSH heading “Arachidonic Acid” (counts retrieved 2026-10-31). 1,328 of them (6.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 11,609 records.
Reviews account for 1,818 records (9.1%) and meta-analyses for 32. Randomized controlled trials number 352 (1.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 11,609 |
| 2000-2009 | 4,202 |
| 2010-2019 | 2,797 |
| 2020 onward | 1,328 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,818 | 9.1% |
| Meta-analyses | 32 | 0.2% |
| Randomized controlled trials | 352 | 1.8% |
Method: PubMed query "Arachidonic Acid"[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.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Arachidonic Acid Metabolites in Cardiovascular and Metabolic Diseases | 2018 | Review article Design not recorded in structured metadata | 365 | cc by PMID 30360467 · DOI · PMC6274989 |
| Arachidonic Acid Metabolism and Kidney Inflammation | 2019 | Review article Design not recorded in structured metadata | 317 | cc by PMID 31357612 · DOI · PMC6695795 |
| The Essentiality of Arachidonic Acid in Infant Development | 2016 | Review article Design not recorded in structured metadata | 268 | cc by PMID 27077882 · DOI · PMC4848685 |
| Crosstalk between arachidonic acid metabolism and glycolysis drives integrated metabolic-inflammatory reprogramming in macrophages | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41522345 · DOI · PMC12781075 |
Arachidonic Acid Metabolites in Cardiovascular and Metabolic Diseases [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Lipid and immune pathways are crucial in the pathophysiology of metabolic and cardiovascular disease.
- Closing excerpt
- We herein present a synopsis of AA metabolism in human health, tissue homeostasis, and immunity, and explore the role of the AA metabolome in diverse pathophysiological conditions and diseases.
- 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 (80 words)
Lipid and immune pathways are crucial in the pathophysiology of metabolic and cardiovascular disease. Arachidonic acid (AA) and its derivatives link nutrient metabolism to immunity and inflammation, thus holding a key role in the emergence and progression of frequent diseases such as obesity, diabetes, non-alcoholic fatty liver disease, and cardiovascular disease. We herein present a synopsis of AA metabolism in human health, tissue homeostasis, and immunity, and explore the role of the AA metabolome in diverse pathophysiological conditions and diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30360467 · DOI · PMC6274989
Arachidonic Acid Metabolism and Kidney Inflammation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP450) enzymes.
- Closing excerpt
- These observations support an extraordinary interest in a wide range of studies on drug interventions aiming to control AA metabolism and kidney inflammation.
- 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 (210 words)
As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP450) enzymes. Based on these three metabolic pathways, AA could be converted into various metabolites that trigger different inflammatory responses. In the kidney, prostaglandins (PG), thromboxane (Tx), leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) are the major metabolites generated from AA. An increased level of prostaglandins (PGs), TxA2 and leukotriene B4 (LTB4) results in inflammatory damage to the kidney. Moreover, the LTB4-leukotriene B4 receptor 1 (BLT1) axis participates in the acute kidney injury via mediating the recruitment of renal neutrophils. In addition, AA can regulate renal ion transport through 19-hydroxystilbenetetraenoic acid (19-HETE) and 20-HETE, both of which are produced by cytochrome P450 monooxygenase. Epoxyeicosatrienoic acids (EETs) generated by the CYP450 enzyme also plays a paramount role in the kidney damage during the inflammation process. For example, 14 and 15-EET mitigated ischemia/reperfusion-caused renal tubular epithelial cell damage. Many drug candidates that target the AA metabolism pathways are being developed to treat kidney inflammation. These observations support an extraordinary interest in a wide range of studies on drug interventions aiming to control AA metabolism and kidney inflammation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31357612 · DOI · PMC6695795
The Essentiality of Arachidonic Acid in Infant Development [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Arachidonic acid (ARA, 20:4n-6) is an n-6 polyunsaturated 20-carbon fatty acid formed by the biosynthesis from linoleic acid (LA, 18:2n-6).
- Closing excerpt
- The amounts and ratios of ARA and DHA needed in infant formula are discussed based on an in depth review of the available scientific evidence.
- 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 (216 words)
Arachidonic acid (ARA, 20:4n-6) is an n-6 polyunsaturated 20-carbon fatty acid formed by the biosynthesis from linoleic acid (LA, 18:2n-6). This review considers the essential role that ARA plays in infant development. ARA is always present in human milk at a relatively fixed level and is accumulated in tissues throughout the body where it serves several important functions. Without the provision of preformed ARA in human milk or infant formula the growing infant cannot maintain ARA levels from synthetic pathways alone that are sufficient to meet metabolic demand. During late infancy and early childhood the amount of dietary ARA provided by solid foods is low. ARA serves as a precursor to leukotrienes, prostaglandins, and thromboxanes, collectively known as eicosanoids which are important for immunity and immune response. There is strong evidence based on animal and human studies that ARA is critical for infant growth, brain development, and health. These studies also demonstrate the importance of balancing the amounts of ARA and DHA as too much DHA may suppress the benefits provided by ARA. Both ARA and DHA have been added to infant formulas and follow-on formulas for more than two decades. The amounts and ratios of ARA and DHA needed in infant formula are discussed based on an in depth review of the available scientific evidence.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27077882 · DOI · PMC4848685
Crosstalk between arachidonic acid metabolism and glycolysis drives integrated metabolic-inflammatory reprogramming in macrophages [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Arachidonic acid (AA)-derived lipid mediators play pivotal roles in inflammation and its resolution.
- Closing excerpt
- This pathway positions 15KPF as a promising therapeutic candidate for inflammatory and metabolic diseases, including ischemia-reperfusion injury, and distinguishes it from synthetic allosteric PKM2 activators such as TEPP-46.
- 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 (191 words)
Arachidonic acid (AA)-derived lipid mediators play pivotal roles in inflammation and its resolution. While glycolysis is a key metabolic pathway determining macrophage polarization, the crosstalk between specific AA metabolites and glycolytic reprogramming remains poorly understood. In this study, we explore whether certain AA metabolites modulate macrophage function through covalent protein modification, with therapeutic implications for myocardial ischemia-reperfusion injury. Unlike conventional specialized pro-resolving mediators (SPMs) that primarily act via receptors, here we identify an endogenous electrophilic AA metabolite, 15-keto-prostaglandin F2α (15KPF), that covalently modifies pyruvate kinase M2 (PKM2) at Cys49. Such interaction enhanced PKM2 tetramerization, suppressed the PKM2/HIF-1α/STAT3 axis, redirected energy metabolism from glycolysis to mitochondrial respiration, and promoted pro-resolving M2 macrophage polarization. Mutated PKM2(C49S) failed to inhibit STAT3 signaling and blocked the effect of 15KPF on M1 to M2 phenotype switch. Moreover, 15KPF reduced infarct size and preserved myocardial integrity in in vivo model. Taken together, covalent 15-keto-PGF2α-PKM2 conjugation represents a self-regulatory mechanism linking AA metabolism to glycolysis to drive macrophage metabolic-inflammatory reprogramming. This pathway positions 15KPF as a promising therapeutic candidate for inflammatory and metabolic diseases, including ischemia-reperfusion injury, and distinguishes it from synthetic allosteric PKM2 activators such as TEPP-46.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41522345 · DOI · PMC12781075
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 P-450 metabolites of arachidonic acid in the control of cardiovascular function [5]
- Research article Phospholipase A2 enzymes [6]
- Research article Epoxygenase pathways of arachidonic acid metabolism [7]
- Research article Arachidonic-acid-derived eicosanoids: roles in biology and immunopathology [8]
- Research article Arachidonic acid as a bioactive molecule [9]
- Research article Docosahexaenoic and arachidonic acid concentrations in human breast milk worldwide [10]
References
- Sonnweber T, Pizzini A, Nairz M, Weiss G, Tancevski I. Arachidonic Acid Metabolites in Cardiovascular and Metabolic Diseases. . 2018. PMID 30360467 · DOI · PMC6274989
- Wang T, Fu X, Chen Q, Patra JK, Wang D, Wang Z, et al.. Arachidonic Acid Metabolism and Kidney Inflammation. . 2019. PMID 31357612 · DOI · PMC6695795
- Hadley KB, Ryan AS, Forsyth S, Gautier S, Salem N. The Essentiality of Arachidonic Acid in Infant Development. . 2016. PMID 27077882 · DOI · PMC4848685
- Cheng Y, Fan N, Zhang X, Zhao W, Xie B, Zhao J, et al.. Crosstalk between arachidonic acid metabolism and glycolysis drives integrated metabolic-inflammatory reprogramming in macrophages. . 2026. PMID 41522345 · DOI · PMC12781075
- Roman RJ. P-450 metabolites of arachidonic acid in the control of cardiovascular function. Physiol Rev. 2002. PMID 11773611 · DOI
- Kudo I, Murakami M. Phospholipase A2 enzymes. Prostaglandins Other Lipid Mediat. 2002. PMID 12432908 · DOI
- Zeldin DC. Epoxygenase pathways of arachidonic acid metabolism. J Biol Chem. 2001. PMID 11451964 · DOI
- Harizi H, Corcuff JB, Gualde N. Arachidonic-acid-derived eicosanoids: roles in biology and immunopathology. Trends Mol Med. 2008. PMID 18774339 · DOI
- Brash AR. Arachidonic acid as a bioactive molecule. J Clin Invest. 2001. PMID 11390413 · DOI · PMC209328
- Brenna JT, Varamini B, Jensen RG, Diersen-Schade DA, Boettcher JA, Arterburn LM. Docosahexaenoic and arachidonic acid concentrations in human breast milk worldwide. Am J Clin Nutr. 2007. PMID 17556680 · 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.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
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.