Cyclooxygenase-dependent platelet aggregation: molecular mechanisms & dependencies

How nutrients influence it

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Human evidence only

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

Aspirin increased 15R-prostaglandin D2 but not 15R-prostaglandin E2 in isolated human leukocytes activated with lipopolysaccharide to induce cyclooxygenase-2, and 15R-prostaglandin D2 inhibited human platelet aggregation induced by the thromboxane receptor agonist U46,619, an effect abrogated by an antagonist of the DP1 prostanoid receptor, so 15R-prostaglandins are novel products of aspirin therapy that may contribute to its antiplatelet and other effects.
15R-prostaglandin D2 → Cyclooxygenase-dependent platelet aggregation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/aspirin-research/30096040.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8", "start_char": 0, "end_char": 1666, "text_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8"}
experimental_model
Radiolabelled substrate and LC-MS analysis of aspirin-acetylated COX-2 products, with human leukocytes and platelet aggregation assays
exposure
Aspirin acetylation, with lipopolysaccharide-induced cyclooxygenase-2 in leukocytes and a thromboxane receptor agonist on platelets
limitations
Shows the acetylated enzyme keeps more of its original chemistry than the HETE story implies, and links the product to a measured platelet effect. Isolated cells rather than treated people.
nutrient_topic
Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
organism
Human
plain_language
One of those mirror-image products is itself an antiplatelet agent, working through a different receptor.
primary_references
[asa-p30096040] Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation. (2019). https://pubmed.ncbi.nlm.nih.gov/30096040/ DOI: 10.1096/fj.201801018r
tissue_or_cell_type
Recombinant enzyme and isolated leukocytes and platelets
Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 299–310
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabelled substrate and LC-MS analysis of aspirin-acetylated COX-2 products, with human leukocytes and platelet aggregation assays · source_derived_draft · unverified_draft
### asa-15r-pgd2-blocks-platelets Aspirin increased 15R-prostaglandin D2 but not 15R-prostaglandin E2 in isolated human leukocytes activated with lipopolysaccharide to induce cyclooxygenase-2, and 15R-prostaglandin D2 inhibited human platelet aggregation induced by the thromboxane receptor agonist U46,619, an effect abrogated by an antagonist of the DP1 prostanoid receptor, so 15R-prostaglandins are novel products of aspirin therapy that may contribute to its antiplatelet and other effects. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: One of those mirror-image products is itself an antiplatelet agent, working through a different receptor. organism: Human tissue_or_cell_type: Recombinant enzyme and isolated leukocytes and platelets experimental_model: Radiolabelled substrate and LC-MS analysis of aspirin-acetylated COX-2 products, with human leukocytes and platelet aggregation assays limitations: Shows the acetylated enzyme keeps more of its original chemistry than the HETE story implies, and links the product to a measured platelet effect. Isolated cells rather than treated people. exposure: Aspirin acetylation, with lipopolysaccharide-induced cyclooxygenase-2 in leukocytes and a thromboxane receptor agonist on platelets evidence_span: {"source_cache": "artifacts/aspirin-research/30096040.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8", "start_char": 0, "end_char": 1666, "text_sha256": "2bd9c817ec4fe31752028634955f604eb00829efc93a72d5fc7e22be7f5739b8"} [asa-p30096040] Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation. (2019). https://pubmed.ncbi.nlm.nih.gov/30096040/ DOI: 10.1096/fj.201801018r
Complete structured claim and evidence
In rabbits lower doses of aspirin produced major inhibition of platelet aggregation and minor inhibition of prostacyclin synthesis while higher doses inhibited both, in humans a dose equivalent to approximately one quarter of one 300 milligram tablet consistently produced major inhibition of cyclooxygenase-dependent platelet aggregation in a pattern similar to that in rabbits where most prostacyclin synthetic capacity was not inhibited, and it took rabbit vasculature over 24 hours to return to control prostacyclin synthetic capacity after a single high dose.
Aspirin / acetylsalicylic acid → Cyclooxygenase-dependent platelet aggregation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/aspirin-research/6156337.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074", "start_char": 0, "end_char": 1502, "text_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074"}
experimental_model
Human and rabbit platelet aggregation with rabbit aortic prostacyclin synthesis measured across aspirin doses
exposure
Graded oral aspirin doses, sampled three hours after dosing, with recovery followed over 24 hours in rabbits
limitations
Sets the dose at which the two tissues start to separate, but the vascular arm is rabbit aorta and the human arm measures aggregation rather than prostacyclin.
nutrient_topic
Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
organism
Human and rabbit
plain_language
About a quarter of a tablet stops the platelets while mostly leaving the vessel wall alone.
primary_references
[asa-p6156337] Effect of oral aspirin dose on platelet aggregation and vascular prostacyclin (PGI2) synthesis in humans and rabbits. (1980). https://pubmed.ncbi.nlm.nih.gov/6156337/ DOI: 10.1097/00005344-198007000-00006
tissue_or_cell_type
Platelets and aorta
Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 390–401
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and rabbit platelet aggregation with rabbit aortic prostacyclin synthesis measured across aspirin doses · source_derived_draft · unverified_draft
### asa-a-quarter-tablet In rabbits lower doses of aspirin produced major inhibition of platelet aggregation and minor inhibition of prostacyclin synthesis while higher doses inhibited both, in humans a dose equivalent to approximately one quarter of one 300 milligram tablet consistently produced major inhibition of cyclooxygenase-dependent platelet aggregation in a pattern similar to that in rabbits where most prostacyclin synthetic capacity was not inhibited, and it took rabbit vasculature over 24 hours to return to control prostacyclin synthetic capacity after a single high dose. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: About a quarter of a tablet stops the platelets while mostly leaving the vessel wall alone. organism: Human and rabbit tissue_or_cell_type: Platelets and aorta experimental_model: Human and rabbit platelet aggregation with rabbit aortic prostacyclin synthesis measured across aspirin doses limitations: Sets the dose at which the two tissues start to separate, but the vascular arm is rabbit aorta and the human arm measures aggregation rather than prostacyclin. exposure: Graded oral aspirin doses, sampled three hours after dosing, with recovery followed over 24 hours in rabbits evidence_span: {"source_cache": "artifacts/aspirin-research/6156337.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074", "start_char": 0, "end_char": 1502, "text_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074"} [asa-p6156337] Effect of oral aspirin dose on platelet aggregation and vascular prostacyclin (PGI2) synthesis in humans and rabbits. (1980). https://pubmed.ncbi.nlm.nih.gov/6156337/ DOI: 10.1097/00005344-198007000-00006
Complete structured claim and evidence

The events it takes part in

A mechanism often involves more than two components. These are the full events, with every participant and its role.

Situations it appears in

Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

Open hypotheses

Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.

This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

Cyclooxygenase-dependent platelet aggregation