{"id":"5fa92dc6-9464-5c3d-afe9-9984ffd3f68a","stable_key":"3279ff78-2460-5064-bfc0-3f2987af85a0:melatonin-mitochondrial-caspase","predicate":"inhibits","statement":"The same experimental mitochondrial pathway reduced downstream caspase activation.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"536b1e75-757f-5fe2-a331-da7a65c2a4d4","mechanism_event_label":"This preclinical injury endpoint is not a demonstrated stroke treatment.","subject":{"id":"1ed52045-0f2b-568c-8b15-150af5bfd17a","slug":"neuronal-mitochondrial-mt1-signaling","display_name":"MT1-associated signaling in experimental neuronal mitochondria","entity_type_key":"cellular_process"},"object":{"id":"99984499-649b-5654-ac40-dbc6dc3d2367","slug":"neuronal-caspase-activation","display_name":"Caspase activation in experimental neuronal injury","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"536b1e75-757f-5fe2-a331-da7a65c2a4d4","stable_key":"3279ff78-2460-5064-bfc0-3f2987af85a0:melatonin-mitochondrial-caspase-event","event_type":"biochemical_relationship","label":"This preclinical injury endpoint is not a demonstrated stroke treatment.","description":"The same experimental mitochondrial pathway reduced downstream caspase activation.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"0f0bc1f1-d18d-5652-bc1d-98f61f7ab65c","slug":"melatonin","display_name":"Melatonin","entity_type_key":"small_molecule"},"role":"local_ligand","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"1ed52045-0f2b-568c-8b15-150af5bfd17a","slug":"neuronal-mitochondrial-mt1-signaling","display_name":"MT1-associated signaling in experimental neuronal mitochondria","entity_type_key":"cellular_process"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"99984499-649b-5654-ac40-dbc6dc3d2367","slug":"neuronal-caspase-activation","display_name":"Caspase activation in experimental neuronal injury","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/melatonin-research/28874589.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"f20a034160c8e4d6022d0334d4ad9177591046f78a397ded41c90165b8847ade\", \"start_char\": 0, \"end_char\": 1091, \"text_sha256\": \"f20a034160c8e4d6022d0334d4ad9177591046f78a397ded41c90165b8847ade\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Neuronal mitochondrial fractionation, signaling and injury experiments","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Organelle synthesis and MT1 signaling; MT1 overexpression in mouse ischemia","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Claims remain within the studied neuronal system; do not infer all human melatonin is mitochondrial or that oral supplements reproduce local synthesis. Transgene expression and endogenous protein identity are not merged.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Melatonin research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"melatonin","display_name":"Melatonin","entity_type_key":"small_molecule"}},{"dimension":"organism","value_text":"Experimental neuronal systems and mice","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"This preclinical injury endpoint is not a demonstrated stroke treatment.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[melatonin-p28874589] Dual role of mitochondria in producing melatonin and driving GPCR signaling to block cytochrome c release. (2017). https://pubmed.ncbi.nlm.nih.gov/28874589/ DOI: 10.1073/pnas.1705768114","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Mitochondrial melatonin/MT1 pathway","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"916ec27d-554c-505d-af49-d8c772879e27","evidence_kind":"source_excerpt","locator":"Lines 552-563","start_line":552,"end_line":563,"excerpt":"### melatonin-mitochondrial-caspase\nThe same experimental mitochondrial pathway reduced downstream caspase activation.\nCondition category: normal\nnutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: This preclinical injury endpoint is not a demonstrated stroke treatment.\norganism: Experimental neuronal systems and mice\ntissue_or_cell_type: Mitochondrial melatonin/MT1 pathway\nexperimental_model: Neuronal mitochondrial fractionation, signaling and injury experiments\nlimitations: Claims remain within the studied neuronal system; do not infer all human melatonin is mitochondrial or that oral supplements reproduce local synthesis. Transgene expression and endogenous protein identity are not merged.\nexposure: Organelle synthesis and MT1 signaling; MT1 overexpression in mouse ischemia\nevidence_span: {\"source_cache\": \"artifacts/melatonin-research/28874589.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"f20a034160c8e4d6022d0334d4ad9177591046f78a397ded41c90165b8847ade\", \"start_char\": 0, \"end_char\": 1091, \"text_sha256\": \"f20a034160c8e4d6022d0334d4ad9177591046f78a397ded41c90165b8847ade\"}\n[melatonin-p28874589] Dual role of mitochondria in producing melatonin and driving GPCR signaling to block cytochrome c release. 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