{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T02:15:40Z","timestamp":1792808140623,"version":"4.5.0"},"posted":{"date-parts":[[2026,6,3]]},"group-title":"Physiology","reference-count":6,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T00:00:00Z","timestamp":1780444800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"name":"US National Institutes of Health (NIH) grants","award":["R01AR079449"],"award-info":[{"award-number":["R01AR079449"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"crossref"}]},{"name":"US National Institutes of Health (NIH) grants","award":["R01AR054396"],"award-info":[{"award-number":["R01AR054396"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"crossref"}]},{"name":"US National Institutes of Health (NIH) grants","award":["R01HD089918"],"award-info":[{"award-number":["R01HD089918"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"crossref"}]},{"name":"US National Institutes of Health (NIH) grants","award":["R01HL171050"],"award-info":[{"award-number":["R01HL171050"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>Cardiomyocytes die and do not regenerate after an injury such as a myocardial infarction (MI), a leading cause of mortality worldwide. Following MI, cardiac fibroblasts (CFs) proliferate and differentiate into myofibroblasts, which then produce increased collagen and extracellular matrix (ECM) leading to fibrosis. Fibrosis can weaken cardiac output via excessive stiffening and interference with electric signal transmission, but can also prevent wall rupture under load (reviewed in (1)). Thus, dampening fibrosis has been investigated as a potential therapeutic intervention. Most mammalian cells possess a single primary cilium involved in intercellular communication. We investigated the role of CF primary cilia in sensing injury signals and initiating fibrotic remodeling. We found that deleting CF cilia reduced fibrosis and improved cardiac output after MI, demonstrating that cilia act as a signaling hub that amplifies the fibrotic response in the injured heart.<\/jats:p>","DOI":"10.64898\/2026.05.30.728594","type":"posted-content","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T12:50:14Z","timestamp":1780491014000},"source":"Crossref","is-referenced-by-count":1,"title":["Primary cilia promote cardiac fibrosis and limit heart function after myocardial infarction"],"prefix":"10.64898","author":[{"given":"Xinyue","family":"Liu","sequence":"first","affiliation":[{"name":"University of Florida, Department of Pharmacology and Therapeutics, Myology Institute, Gainesville, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandra","family":"Norris","sequence":"additional","affiliation":[{"name":"University of Florida, Department of Pharmacology and Therapeutics, Myology Institute, Gainesville, FL, USA"},{"name":"Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ambili","family":"Appu","sequence":"additional","affiliation":[{"name":"University of Florida, Department of Pharmacology and Therapeutics, Myology Institute, Gainesville, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily","family":"Wilson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, University of California, San Francisco, San Francisco, CA, USA"},{"name":"Center for Biosignal Research, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, University of California, San Francisco, San Francisco, CA, USA"},{"name":"Center for Biosignal Research, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey","family":"Olgin","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, University of California, San Francisco, San Francisco, CA, USA"},{"name":"Center for Biosignal Research, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6512-320X","authenticated-orcid":false,"given":"Jeremy","family":"Reiter","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA"},{"name":"Chan Zuckerberg Biohub, San Francisco, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5148-8219","authenticated-orcid":false,"given":"Daniel","family":"Kopinke","sequence":"additional","affiliation":[{"name":"University of Florida, Department of Pharmacology and Therapeutics, Myology Institute, Gainesville, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026060604251196000_2026.05.30.728594v1.1","doi-asserted-by":"publisher","DOI":"10.1007\/s00441-016-2431-9"},{"key":"2026060604251196000_2026.05.30.728594v1.2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.117.028752"},{"key":"2026060604251196000_2026.05.30.728594v1.3","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2017.06.035"},{"key":"2026060604251196000_2026.05.30.728594v1.4","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-023-39506-1"},{"key":"2026060604251196000_2026.05.30.728594v1.5","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-022-04989-3"},{"key":"2026060604251196000_2026.05.30.728594v1.6","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.119.045115"}],"container-title":[],"original-title":[],"link":[{"URL":"https:\/\/syndication.highwire.org\/content\/doi\/10.64898\/2026.05.30.728594","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T11:25:18Z","timestamp":1780745118000},"score":1,"resource":{"primary":{"URL":"http:\/\/biorxiv.org\/lookup\/doi\/10.64898\/2026.05.30.728594"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,6,3]]},"references-count":6,"URL":"https:\/\/doi.org\/10.64898\/2026.05.30.728594","relation":{},"subject":[],"published":{"date-parts":[[2026,6,3]]},"subtype":"preprint"}}