{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T19:22:09Z","timestamp":1792178529138,"version":"4.4.0"},"reference-count":54,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"831","funder":[{"DOI":"10.13039\/100021828","name":"German Academic Exchange Service","doi-asserted-by":"publisher","award":["GSSP 57243780"],"award-info":[{"award-number":["GSSP 57243780"]}],"id":[{"id":"10.13039\/100021828","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["KFO311 WO 552\/11-1"],"award-info":[{"award-number":["KFO311 WO 552\/11-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["KFO311 WO 552\/11-2"],"award-info":[{"award-number":["KFO311 WO 552\/11-2"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["KFO311 ZW 64\/7-1"],"award-info":[{"award-number":["KFO311 ZW 64\/7-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["FA 330\/12-3"],"award-info":[{"award-number":["FA 330\/12-3"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2026,1,7]]},"abstract":"<jats:p>\n                    Tissue repair after myocardial infarction entails a vigorous angiogenic response that mitigates scarring and worsening of heart function. Angiogenesis in the infarct wound is guided by incompletely defined myeloid cell\u2013endothelial cell interactions. Here, we identify the 75\u2013amino acid microprotein BRICK1 (BRK1) as an indispensable driver of postinfarction angiogenesis in a mouse model of reperfused myocardial infarction. We show that BRK1 is preferentially expressed by myeloid cells and translocates to the extracellular space after myocardial infarction in mice and humans. As a subunit of the intracellular actin-regulatory WAVE complex, BRK1 was not previously known to function outside the cell. We find that BRK1 is not actively secreted but released during myeloid cell death. Cre-\n                    <jats:italic toggle=\"yes\">loxP<\/jats:italic>\n                    \u2013driven myeloid cell\u2013selective genetic deletion of\n                    <jats:italic toggle=\"yes\">Brk1<\/jats:italic>\n                    or antibody-mediated neutralization of extracellular BRK1 impaired microvessel formation in the infarct border zone and resulted in severe postinfarction heart failure in mice. Conversely, treatment with recombinant BRK1 preserved heart function in infarcted mice. Mechanistically, BRK1 induced an angiogenic phenotype in human cardiac endothelial cells by signaling via the small GTPase Ras-related protein Rap-1 and mitogen-activated protein kinases 1 and 3 to promote retinoblastoma protein hyperphosphorylation and E2F transcription factor activation. BRK1 thus emerges as an angiogenic factor linking myeloid cell death to ischemic tissue repair, potentially enabling a protein-based therapy for myocardial infarction.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adx2876","type":"journal-article","created":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T18:58:20Z","timestamp":1767812300000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":3,"title":["Extracellular BRICK1 drives heart repair after myocardial infarction in mice"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1076-5272","authenticated-orcid":true,"given":"Felix","family":"Polten","sequence":"first","affiliation":[{"name":"Division of Molecular and Translational Cardiology, Hans Borst Center for Heart and Stem Cell Research, Hannover Medical School, 30625 Hannover, Germany."},{"name":"Department of Cardiology and Angiology, Hannover Medical School, 30625 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Applied Anatomy, Hannover Medical School, 30625 Hannover, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7767-1556","authenticated-orcid":true,"given":"Nils","family":"Kriedemann","sequence":"additional","affiliation":[{"name":"Leibniz Research Laboratories for Biotechnology and Artificial Organs, Department of Cardiothoracic, Transplantation, and Vascular Surgery, Hannover Medical School, 30625 Hannover, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4656-0770","authenticated-orcid":true,"given":"Robert","family":"Zweigerdt","sequence":"additional","affiliation":[{"name":"Leibniz Research Laboratories for Biotechnology and Artificial Organs, Department of Cardiothoracic, Transplantation, and Vascular Surgery, Hannover Medical School, 30625 Hannover, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4360-1511","authenticated-orcid":true,"given":"Thomas","family":"Thum","sequence":"additional","affiliation":[{"name":"Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School, 30625 Hannover, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9341-117X","authenticated-orcid":true,"given":"Johann","family":"Bauersachs","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9404-9822","authenticated-orcid":true,"given":"Hans W.","family":"Niessen","sequence":"additional","affiliation":[{"name":"Department of Pathology and Department of Cardiac Surgery, Institute for Cardiovascular Research, Amsterdam University Medical Center, 1007 MB Amsterdam, Netherlands."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4384-1267","authenticated-orcid":true,"given":"Andrew L.","family":"Koenig","sequence":"additional","affiliation":[{"name":"Center for Cardiovascular Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1948-9945","authenticated-orcid":true,"given":"Kory J.","family":"Lavine","sequence":"additional","affiliation":[{"name":"Center for Cardiovascular Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8444-0940","authenticated-orcid":true,"given":"Andreas","family":"Pich","sequence":"additional","affiliation":[{"name":"Core Unit Proteomics and Institute of Toxicology, 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