Human prostaglandin D2 receptor 1 / PTGDR: molecular mechanisms & dependencies

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

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

Where it participates (unsigned role)

In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion.
Laropiprant / MK-0524 → Cutaneous perfusion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger)
evidence_span
{"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"}
experimental_model
Mouse receptor pharmacology with separate healthy-human flushing study
exposure
Nicotinic acid with or without the DP1 antagonist MK-0524
limitations
Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component.
nutrient_topic
Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
organism
Homo sapiens
plain_language
Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.
primary_references
[nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
tissue_or_cell_type
Skin perfusion
Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1361–1373
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse receptor pharmacology with separate healthy-human flushing study · source_derived_draft · unverified_draft
### nia-clin-dp1-human-flush In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes. organism: Homo sapiens tissue_or_cell_type: Skin perfusion experimental_model: Mouse receptor pharmacology with separate healthy-human flushing study limitations: Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component. exposure: Nicotinic acid with or without the DP1 antagonist MK-0524 cross_nutrient: Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"} [nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
Complete structured claim and evidence
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

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.

Human prostaglandin D2 receptor 1 / PTGDR