{"id":"79cb8a3a-cf91-51b0-b61e-d92d1e260cf4","stable_key":"ff370329-68a3-573d-96ee-597de78a3967:api-sasp","predicate":"decreases_in_recorded_comparison","statement":"Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.","claim_class":"observational","status":"source_recorded","evidence_grade":"ungraded","direction":"negative","is_public":true,"mechanism_event_id":"7abc5f1d-8af2-5053-bd1a-4c605d954211","mechanism_event_label":"Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.","subject":{"id":"4425961f-4764-56d3-9887-87e47749379b","slug":"apigenin","display_name":"Apigenin","entity_type_key":"small_molecule"},"object":{"id":"fcc8cc95-bb72-5a38-b74e-dc3f5e9fea2f","slug":"api-human-fibroblast-sasp","display_name":"Senescence-associated secretory phenotype in apigenin-treated human fibroblasts","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"7abc5f1d-8af2-5053-bd1a-4c605d954211","stable_key":"ff370329-68a3-573d-96ee-597de78a3967:api-sasp-event","event_type":"experimental_observation","label":"Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.","description":"### api-sasp\n\nApigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.\nPrimary abstract scope. Suppression was linked to IL-1/IRAK/p38/NF-kappaB signaling; this does not prove senolysis.\nModel and exposure: Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments.\nLimitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.\nReference: Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | 2017 | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"4425961f-4764-56d3-9887-87e47749379b","slug":"apigenin","display_name":"Apigenin","entity_type_key":"small_molecule"},"role":"tested factor","stoichiometry":null,"state_label":"Apigenin in senescent fibroblasts","sequence_order":0,"notes":""},{"entity":{"id":"fcc8cc95-bb72-5a38-b74e-dc3f5e9fea2f","slug":"api-human-fibroblast-sasp","display_name":"Senescence-associated secretory phenotype in apigenin-treated human fibroblasts","entity_type_key":"cellular_process"},"role":"measured outcome","stoichiometry":null,"state_label":"decrease","sequence_order":1,"notes":""},{"entity":{"id":"2d782fde-a46c-5671-a67a-d7ebb51d06b8","slug":"human-il1a","display_name":"Human interleukin-1 alpha / IL1A","entity_type_key":"cytokine"},"role":"upstream SASP signaling","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"be5bf77b-c965-502a-be1b-b6729f62441a","slug":"human-irak1","display_name":"Human interleukin-1 receptor-associated kinase 1 / IRAK1","entity_type_key":"protein"},"role":"signaling component","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""},{"entity":{"id":"975f5a30-c260-529e-a194-deab37fc7efe","slug":"human-irak4","display_name":"Human interleukin-1 receptor-associated kinase 4 / IRAK4","entity_type_key":"protein"},"role":"signaling component","stoichiometry":null,"state_label":"","sequence_order":4,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_contrast","value_text":"{\"intervention\": \"Apigenin in senescent fibroblasts\", \"comparator\": \"Senescent vehicle controls\", \"endpoint\": \"Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.\", \"effect_direction\": \"decrease\", \"combination\": \"single\", \"conditions\": []}","comparator":null,"unit":null,"notes":"Explicit extracted experimental comparison; recorded from source.","entity":null},{"dimension":"experimental_model","value_text":"Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"interpretation_status","value_text":"Recorded from source with stated access limits; ungraded, not independent replication.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Apigenin collection; exact intervention and molecular form govern interpretation.","comparator":null,"unit":null,"notes":"","entity":{"slug":"apigenin","display_name":"Apigenin","entity_type_key":"small_molecule"}},{"dimension":"plain_language","value_text":"Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"source_locator","value_text":"Reviewed reference api-sasp; Primary abstract scope. Suppression was linked to IL-1/IRAK/p38/NF-kappaB signaling; this does not prove senolysis.","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"ffaea08e-4eaf-5595-837d-0760c4362d19","evidence_kind":"source_excerpt","locator":"Lines 752-758","start_line":752,"end_line":758,"excerpt":"### api-sasp\n\nApigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.\nPrimary abstract scope. Suppression was linked to IL-1/IRAK/p38/NF-kappaB signaling; this does not prove senolysis.\nModel and exposure: Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments.\nLimitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.\nReference: Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | 2017 | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.","model_system":"Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments.","directness":"reported_statement","verification_status":"source_recorded","notes":"Original paraphrase in the retained reviewed reference, not a verbatim primary-paper quotation. Access level is explicit.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"54eac90b-add1-5f56-9036-d900307c5697","stable_key":"import-ff370329-68a3-573d-96ee-597de78a3967","title":"Apigenin: detailed mechanisms of action (reviewed 10 October 2026)","document_type":"imported_text","citation_label":"AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed.","file_path":"","sha256":"ede6e5c6b91d66b66844f2ff667a7f8303d9ac1281f15dc09db703f7de4da942","revision_id":"b41a39a2-0197-549c-97a5-1765e6696931","review_status":"source_recorded","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}