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Regurgitant flow induced shear stress disrupts Ca\n                      <jats:sup>2+<\/jats:sup>\n                      homeostasis in atrial cardiomyocytes. Overloaded Ca\n                      <jats:sup>2+<\/jats:sup>\n                      is a crucial regulator of endoplasmic reticulum stress-mediated apoptosis, although the regulatory mechanisms remain unclear. We aimed to explore the relationship between shear stress and Ca\n                      <jats:sup>2+<\/jats:sup>\n                      homeostasis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>\n                      Through employing an in vitro model replicating atrial cardiomyocytes during mitral regurgitation, we observed that shear stress increased Ca\n                      <jats:sup>2+<\/jats:sup>\n                      oscillation and the amplitude of Ca\n                      <jats:sup>2+<\/jats:sup>\n                      waves through extracellular Ca\n                      <jats:sup>2+<\/jats:sup>\n                      influx. Suppression of mechanosensitive Ca\n                      <jats:sup>2+<\/jats:sup>\n                      channels or store-operated calcium entry resulted in decreased intracellular Ca\n                      <jats:sup>2+<\/jats:sup>\n                      concentration and oscillation. Conversely, the inhibition of voltage-gated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      channels did not significantly impact the Ca\n                      <jats:sup>2+<\/jats:sup>\n                      concentration. Remarkably, shear stress elevated the expression of endoplasmic reticulum stress and apoptosis-related proteins in HL-1 cells in a time-dependent manner. Also, in a novel rodent mitral regurgitation model, shear stress increased apoptosis and endoplasmic reticulum stress expression compared to sham rats.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our findings underscore that shear stress induces apoptosis through mechanosensitive and store-operated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      channels, leading to Ca\n                      <jats:sup>2+<\/jats:sup>\n                      overload and endoplasmic reticulum stress. Understanding the mechanisms behind shear stress-disturbed Ca\n                      <jats:sup>2+<\/jats:sup>\n                      homeostasis may enhance the treatment of mitral regurgitation-induced heart failure.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s40659-026-00671-4","type":"journal-article","created":{"date-parts":[[2026,2,8]],"date-time":"2026-02-08T07:44:57Z","timestamp":1770536697000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Shear stress-induced Ca2+ influx triggers endoplasmic reticulum stress and cardiomyocyte apoptosis: implications for mitral regulation"],"prefix":"10.1186","volume":"59","author":[{"given":"Wei-Ting","family":"Chang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun-Ming","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan-E","family":"Mo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jhih-Yuan","family":"Shih","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0310-0675","authenticated-orcid":false,"given":"Wen-Tai","family":"Chiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,2,8]]},"reference":[{"issue":"1-2","key":"671_CR1","doi-asserted-by":"publisher","first-page":"69","DOI":"10.1159\/000452682","volume":"58","author":"H Asai","year":"2017","unstructured":"Asai H, Shingu Y, Yamakawa T, Niwano H, Wakasa S, Ooka T, et al. 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