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: 3 complete abstracts (655 words), 9 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 unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
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: A2, Thromboxane; Rabbit Aorta Contracting Substance.
Where it fits in the MeSH classification
- Broader topics
- Thromboxanes
Research landscape
PubMed indexes 5,714 records tagged with the MeSH heading “Thromboxane A2” (counts retrieved 2026-10-31). 132 of them (2.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 4,198 records.
Reviews account for 542 records (9.5%) and meta-analyses for 1. Randomized controlled trials number 127 (2.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 4,198 |
| 2000-2009 | 921 |
| 2010-2019 | 463 |
| 2020 onward | 132 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 542 | 9.5% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 127 | 2.2% |
Method: PubMed query "Thromboxane A2"[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 |
|---|---|---|---|---|
| Aspirin blocks formation of metastatic intravascular niches by inhibiting platelet-derived COX-1/thromboxane A2 | 2019 | Research article Design not recorded in structured metadata | 190 | cc by PMID 30907747 · DOI · PMC6486338 |
| Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity | 2025 | Research article Design not recorded in structured metadata | 112 | cc by PMID 40044852 · DOI · PMC12018268 |
| Multi-omics study of silicosis reveals the potential therapeutic targets PGD2 and TXA2 | 2021 | Research article Design not recorded in structured metadata | 75 | cc by PMID 33500731 · DOI · PMC7797695 |
Aspirin blocks formation of metastatic intravascular niches by inhibiting platelet-derived COX-1/thromboxane A2 [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Because metastasis is associated with the majority of cancer-related deaths, its prevention is a clinical aspiration.
- Closing excerpt
- Thus, platelet-derived TXA2 orchestrates the generation of a favorable intravascular metastatic niche that promotes tumor cell seeding and identifies COX-1/TXA2 signaling as a target for the prevention of metastasis.
- 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)
Because metastasis is associated with the majority of cancer-related deaths, its prevention is a clinical aspiration. Prostanoids are a large family of bioactive lipids derived from the activity of cyclooxygenase-1 (COX-1) and COX-2. Aspirin impairs the biosynthesis of all prostanoids through the irreversible inhibition of both COX isoforms. Long-term administration of aspirin leads to reduced distant metastases in murine models and clinical trials, but the COX isoform, downstream prostanoid, and cell compartment responsible for this effect are yet to be determined. Here, we have shown that aspirin dramatically reduced lung metastasis through inhibition of COX-1 while the cancer cells remained intravascular and that inhibition of platelet COX-1 alone was sufficient to impair metastasis. Thromboxane A2 (TXA2) was the prostanoid product of COX-1 responsible for this antimetastatic effect. Inhibition of the COX-1/TXA2 pathway in platelets decreased aggregation of platelets on tumor cells, endothelial activation, tumor cell adhesion to the endothelium, and recruitment of metastasis-promoting monocytes/macrophages, and diminished the formation of a premetastatic niche. Thus, platelet-derived TXA2 orchestrates the generation of a favorable intravascular metastatic niche that promotes tumor cell seeding and identifies COX-1/TXA2 signaling as a target for the prevention of metastasis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30907747 · DOI · PMC6486338
Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Metastasis is the spread of cancer cells from primary tumours to distant organs and is the cause of 90% of cancer deaths globally1,2.
- Closing excerpt
- These findings reveal a novel immunosuppressive pathway that limits T cell immunity to cancer metastasis, providing mechanistic insights into the anti-metastatic activity of aspirin and paving the way for more effective anti-metastatic immunotherapies.
- 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 (218 words)
Metastasis is the spread of cancer cells from primary tumours to distant organs and is the cause of 90% of cancer deaths globally1,2. Metastasizing cancer cells are uniquely vulnerable to immune attack, as they are initially deprived of the immunosuppressive microenvironment found within established tumours3. There is interest in therapeutically exploiting this immune vulnerability to prevent recurrence in patients with early cancer at risk of metastasis. Here we show that inhibitors of cyclooxygenase 1 (COX-1), including aspirin, enhance immunity to cancer metastasis by releasing T cells from suppression by platelet-derived thromboxane A2 (TXA2). TXA2 acts on T cells to trigger an immunosuppressive pathway that is dependent on the guanine exchange factor ARHGEF1, suppressing T cell receptor-driven kinase signalling, proliferation and effector functions. T cell-specific conditional deletion of Arhgef1 in mice increases T cell activation at the metastatic site, provoking immune-mediated rejection of lung and liver metastases. Consequently, restricting the availability of TXA2 using aspirin, selective COX-1 inhibitors or platelet-specific deletion of COX-1 reduces the rate of metastasis in a manner that is dependent on T cell-intrinsic expression of ARHGEF1 and signalling by TXA2 in vivo. These findings reveal a novel immunosuppressive pathway that limits T cell immunity to cancer metastasis, providing mechanistic insights into the anti-metastatic activity of aspirin and paving the way for more effective anti-metastatic immunotherapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40044852 · DOI · PMC12018268
Multi-omics study of silicosis reveals the potential therapeutic targets PGD2 and TXA2 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Rationale: Silicosis is a severe occupational lung disease.
- Closing excerpt
- By blocking the receptors of these two prostanoids, Ramatroban may be a novel potential therapeutic drug to inhibit the progression of silicosis.
- 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 (246 words)
Rationale: Silicosis is a severe occupational lung disease. Current treatments for silicosis have highly limited availability (i.e., lung transplantation) or, do not effectively prolong patient survival time (i.e., lung lavage). There is thus an urgent clinical need for effective drugs to retard the progression of silicosis. Methods: To systematically characterize the molecular changes associated with silicosis and to discover potential therapeutic targets, we conducted a transcriptomics analysis of human lung tissues acquired during transplantation, which was integrated with transcriptomics and metabolomics analyses of silicosis mouse lungs. The results from the multi-omics analyses were then verified by qPCR, western blot, and immunohistochemistry. The effect of Ramatroban on the progression of silicosis was evaluated in a silica-induced mouse model. Results: Wide metabolic alterations were found in lungs from both human patients and mice with silicosis. Targeted metabolite quantification and validation of expression of their synthases revealed that arachidonic acid (AA) pathway metabolites, prostaglandin D2 (PGD2) and thromboxane A2 (TXA2), were significantly up-regulated in silicosis lungs. We further examined the effect of Ramatroban, a clinical antagonist of both PGD2 and TXA2 receptors, on treating silicosis using a mouse model. The results showed that Ramatroban significantly alleviated silica-induced pulmonary inflammation, fibrosis, and cardiopulmonary dysfunction compared with the control group. Conclusion: Our results revealed the importance of AA metabolic reprogramming, especially PGD2 and TXA2 in the progression of silicosis. By blocking the receptors of these two prostanoids, Ramatroban may be a novel potential therapeutic drug to inhibit the progression of silicosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33500731 · DOI · PMC7797695
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 Pharmacology and endogenous roles of prostaglandin endoperoxides, thromboxane A2, and prostacyclin [4]
- Research article Thromboxane A2: physiology/pathophysiology, cellular signal transduction and pharmacology [5]
- Research article Clinical implications of prostaglandin and thromboxane A2 formation (1) [6]
- Research article Mechanisms of platelet activation: thromboxane A2 as an amplifying signal for other agonists [7]
- Research article The prostacyclin--thromboxane A2 balance: pathophysiological and therapeutic implications [8]
- Research article Aspirin resistance: definition, mechanisms and clinical read-outs [9]
References
- Lucotti S, Cerutti C, Soyer M, Gil-Bernabé AM, Gomes AL, Allen PD, et al.. Aspirin blocks formation of metastatic intravascular niches by inhibiting platelet-derived COX-1/thromboxane A2. . 2019. PMID 30907747 · DOI · PMC6486338
- Yang J, Yamashita-Kanemaru Y, Morris BI, Contursi A, Trajkovski D, Xu J, et al.. Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity. . 2025. PMID 40044852 · DOI · PMC12018268
- Pang J, Qi X, Luo Y, Li X, Shu T, Li B, et al.. Multi-omics study of silicosis reveals the potential therapeutic targets PGD2 and TXA2. . 2021. PMID 33500731 · DOI · PMC7797695
- Moncada S, Vane JR. Pharmacology and endogenous roles of prostaglandin endoperoxides, thromboxane A2, and prostacyclin. Pharmacol Rev. 1978. PMID 116251 · DOI
- Nakahata N. Thromboxane A2: physiology/pathophysiology, cellular signal transduction and pharmacology. Pharmacol Ther. 2008. PMID 18374420 · DOI
- Oates JA, FitzGerald GA, Branch RA, Jackson EK, Knapp HR, Roberts LJ. Clinical implications of prostaglandin and thromboxane A2 formation (1). N Engl J Med. 1988. PMID 3045550 · DOI
- FitzGerald GA. Mechanisms of platelet activation: thromboxane A2 as an amplifying signal for other agonists. Am J Cardiol. 1991. PMID 1892057 · DOI
- Bunting S, Moncada S, Vane JR. The prostacyclin--thromboxane A2 balance: pathophysiological and therapeutic implications. Br Med Bull. 1983. PMID 6354352 · DOI
- Patrono C. Aspirin resistance: definition, mechanisms and clinical read-outs. J Thromb Haemost. 2003. PMID 12911581 · 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.