{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T15:19:05Z","timestamp":1780759145552,"version":"3.54.1"},"reference-count":57,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Genomic and Precision Medicine"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Spontaneous coronary artery dissection (SCAD) is an uncommon cause of myocardial infarction that disproportionately affects women, particularly during pregnancy and the peripartum period. Limited understanding of its underlying pathophysiology hinders the development of effective preventive and therapeutic strategies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>This study investigated associations between genetically predicted circulating proteins and tissue-specific RNA levels with genetically predicted SCAD risk using Mendelian randomization and Bayesian colocalization. Genetic scores for &gt;1500 circulating proteins were derived from the UK Biobank (N=34\u2009557) and deCODE (N=35\u2009559). Scores for 13\u2009848 gene transcripts in arterial and fibroblast tissues were generated from Genotype-Tissue Expression data. Associations between these scores and SCAD were assessed in a genome-wide association study meta-analysis of 1917 individuals with SCAD and 9292 controls. Findings were validated in vitro using mass spectrometry-based proteomic analysis of extracellular vesicles from 50 patients with SCAD and 50 healthy controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>Genetic associations of 4 circulating proteins with SCAD (AFAP1 [actin filament\u2013associated protein 1], ECM1 [extracellular matrix protein 1], SPON1 [spondin 1], and STAT6 [signal transducer and activator of transcription 6]) were identified. Two were supported by gene expression data (AFAP1 and ECM1), and one by tissue-specific Bayesian colocalization analyses (ECM1). Protein interaction mapping identified potential shared pathways through the JAK-STAT (Janus kinases and signal transducers and activators of transcription) signaling pathway and inflammatory regulation. Mass spectrometry-based proteomic analysis demonstrated that ECM1 was significantly upregulated in SCAD cases versus controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Integrative analysis of proteomic, transcriptomic, and experimental data revealed 4 circulating proteins genetically associated with SCAD risk, with ECM1 emerging as a key protein with a likely causal role in SCAD pathogenesis. These findings highlight biological pathways for mechanistic studies and protein targets for potential therapeutic interventions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circgen.125.005330","type":"journal-article","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T10:00:31Z","timestamp":1769680831000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["Genetic Association of Circulating Proteins and Gene Transcripts With Spontaneous Coronary Artery Dissection"],"prefix":"10.1161","volume":"19","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2654-8117","authenticated-orcid":true,"given":"Maddalena","family":"Ardissino","sequence":"first","affiliation":[{"name":"Medical Research Council Laboratory of Medical Sciences, Imperial College London, United Kingdom (M.A., J.S.W., A.M.)."},{"name":"British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care (M.A., A.S.B.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-6021-2093","authenticated-orcid":true,"given":"Alec P.","family":"Morley","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine (A.P.M.)"},{"name":"Gonville and Caius College (A.P.M.), University of Cambridge, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0043-0812","authenticated-orcid":true,"given":"Buu","family":"Truong","sequence":"additional","affiliation":[{"name":"Program in Medical &amp; Population Genetics &amp; Cardiovascular Disease Initiative, Broad Institute of Harvard &amp; MIT, Cambridge, MA (B.T., A. 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