{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T05:27:52Z","timestamp":1769578072674,"version":"3.49.0"},"reference-count":53,"publisher":"Public Library of Science (PLoS)","issue":"4","license":[{"start":{"date-parts":[[2025,4,7]],"date-time":"2025-04-07T00:00:00Z","timestamp":1743984000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS ONE"],"abstract":"<jats:p>Physiological cardiac hypertrophy is a compensatory remodeling of the heart in response to stimuli such as exercise training or pregnancy that is reversible and well-tolerated. We previously described how the activating transcription factor 6 (ATF6) proteins, ATF6\u03b1 and ATF6\u03b2, were required for pathological hypertrophy in response to hemodynamic stress. Here, we examine the functional roles of both ATF6 proteins in the context of exercise-induced physiological hypertrophy. After 20 days of swim training, we found differential roles: whole body gene-deleted mice lacking ATF6\u03b1 had an attenuated hypertrophic response compared to wild-type mice but those lacking ATF6\u03b2 did not. Additionally, mice lacking ATF6\u03b1 displayed ventricular dilation and reduced fractional shortening after swimming. While we observed no differences in the expression of downstream UPR signaling between the exercise groups, mice lacking ATF6\u03b1 showed enhanced phosphorylation of extracellular signal-regulated kinase 1\/2 (ERK1\/2). Thus, in response to swim training, loss of ATF6\u03b2 did not hinder the development of physiological hypertrophy, but loss of ATF6\u03b1 resulted in significantly reduced cardiac fractional shortening.<\/jats:p>","DOI":"10.1371\/journal.pone.0320178","type":"journal-article","created":{"date-parts":[[2025,4,7]],"date-time":"2025-04-07T21:16:36Z","timestamp":1744060596000},"page":"e0320178","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":1,"title":["ATF6\u03b2 is not essential for the development of physiological cardiac hypertrophy"],"prefix":"10.1371","volume":"20","author":[{"given":"Emery","family":"Davis","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8037-8940","authenticated-orcid":true,"given":"Mohammad-Reza","family":"Shokri","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1073-6834","authenticated-orcid":true,"given":"Mary B.","family":"Rowland","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"York","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Caroline T.","family":"Cohen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anna Grace","family":"Johnson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-5447-7487","authenticated-orcid":true,"given":"Patrick E.","family":"Moore","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Saige","family":"Schweitzer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jon","family":"Sin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6589-1025","authenticated-orcid":true,"given":"Chuong","family":"Bui","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1453-9675","authenticated-orcid":true,"given":"Robert N.","family":"Correll","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"340","published-online":{"date-parts":[[2025,4,7]]},"reference":[{"issue":"6","key":"pone.0320178.ref001","doi-asserted-by":"crossref","first-page":"697","DOI":"10.1161\/01.RES.45.6.697","article-title":"The cardiac hypertrophy process. 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