{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T03:20:35Z","timestamp":1791429635431,"version":"4.3.3"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2020,7,9]],"date-time":"2020-07-09T00:00:00Z","timestamp":1594252800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Grants-in-Aid for Scientific Research","award":["26221302"],"award-info":[{"award-number":["26221302"]}]},{"name":"Grants-in-Aid for Scientific Research","award":["15K01720"],"award-info":[{"award-number":["15K01720"]}]},{"name":"Grants-in-Aid for Scientific Research","award":["16K07119"],"award-info":[{"award-number":["16K07119"]}]},{"name":"Grants-in-Aid for Scientific Research","award":["17K08339"],"award-info":[{"award-number":["17K08339"]}]},{"name":"Early-Career Scientists","award":["18K18400"],"award-info":[{"award-number":["18K18400"]}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,3,21]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Cardiac hypertrophy is a compensatory response to pressure overload, leading to heart failure. Recent studies have demonstrated that Rho is immediately activated in left ventricles after pressure overload and that Rho signalling plays crucial regulatory roles in actin cytoskeleton rearrangement during cardiac hypertrophic responses. However, the mechanisms by which Rho and its downstream proteins control actin dynamics during hypertrophic responses remain not fully understood. In this study, we identified the pivotal roles of mammalian homologue of Drosophila diaphanous (mDia) 1, a Rho-effector molecule, in pressure overload-induced ventricular hypertrophy.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results\u2003<\/jats:title>\n                  <jats:p>Male wild-type (WT) and mDia1-knockout (mDia1KO) mice (10\u201312\u2009weeks old) were subjected to a transverse aortic constriction (TAC) or sham operation. The heart weight\/tibia length ratio, cardiomyocyte cross-sectional area, left ventricular wall thickness, and expression of hypertrophy-specific genes were significantly decreased in mDia1KO mice 3\u2009weeks after TAC, and the mortality rate was higher at 12\u2009weeks. Echocardiography indicated that mDia1 deletion increased the severity of heart failure 8\u2009weeks after TAC. Importantly, we could not observe apparent defects in cardiac hypertrophic responses in mDia3-knockout mice. Microarray analysis revealed that mDia1 was involved in the induction of hypertrophy-related genes, including immediate early genes, in pressure overloaded hearts. Loss of mDia1 attenuated activation of the mechanotransduction pathway in TAC-operated mice hearts. We also found that mDia1 was involved in stretch-induced activation of the mechanotransduction pathway and gene expression of c-fos in neonatal rat ventricular cardiomyocytes (NRVMs). mDia1 regulated the filamentous\/globular (F\/G)-actin ratio in response to pressure overload in mice. Additionally, increases in nuclear myocardin-related transcription factors and serum response factor were perturbed in response to pressure overload in mDia1KO mice and to mechanical stretch in mDia1 depleted NRVMs.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion\u2003<\/jats:title>\n                  <jats:p>mDia1, through actin dynamics, is involved in compensatory cardiac hypertrophy in response to pressure overload.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvaa206","type":"journal-article","created":{"date-parts":[[2020,7,3]],"date-time":"2020-07-03T11:11:05Z","timestamp":1593774665000},"page":"1103-1117","source":"Crossref","is-referenced-by-count":12,"title":["Disruption of actin dynamics regulated by Rho effector mDia1 attenuates pressure overload-induced cardiac hypertrophic responses and exacerbates dysfunction"],"prefix":"10.1093","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2769-5338","authenticated-orcid":false,"given":"Ichitaro","family":"Abe","sequence":"first","affiliation":[{"name":"Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7102-784X","authenticated-orcid":false,"given":"Takeshi","family":"Terabayashi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0429-1899","authenticated-orcid":false,"given":"Katsuhiro","family":"Hanada","sequence":"additional","affiliation":[{"name":"Clinical Engineering Research Center, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2451-5845","authenticated-orcid":false,"given":"Hidekazu","family":"Kondo","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2156-0598","authenticated-orcid":false,"given":"Yasushi","family":"Teshima","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yumi","family":"Ishii","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miho","family":"Miyoshi","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4528-5516","authenticated-orcid":false,"given":"Shintaro","family":"Kira","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shotaro","family":"Saito","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hasama, Yufu, Oita 879-5593, 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