{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T04:19:11Z","timestamp":1791433151683,"version":"4.3.3"},"reference-count":52,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"14","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Heart failure (HF) is a leading cause of morbidity and mortality worldwide. RNA-binding proteins are identified as regulators of cardiac disease; DDX5 (dead-box helicase 5) is a master regulator of many RNA processes, although its function in heart physiology remains unclear.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              We assessed DDX5 expression in human failing hearts and a mouse HF model. To study the function of DDX5 in heart, we engineered cardiomyocyte-specific\n              <jats:italic toggle=\"yes\">Ddx5<\/jats:italic>\n              knockout mice. We overexpressed DDX5 in cardiomyocytes using adeno-associated virus serotype 9 and performed transverse aortic constriction to establish the murine HF model. The mechanisms underlined were subsequently investigated using immunoprecipitation\u2013mass spectrometry, RNA-sequencing, alternative splicing analysis, and RNA immunoprecipitation sequencing.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              We screened transcriptome databases of murine HF and human dilated cardiomyopathy samples and found that DDX5 was significantly downregulated in both. Cardiomyocyte-specific deletion of\n              <jats:italic toggle=\"yes\">Ddx5<\/jats:italic>\n              resulted in HF with reduced cardiac function, an enlarged heart chamber, and increased fibrosis in mice. DDX5 overexpression improved cardiac function and protected against adverse cardiac remodeling in mice with transverse aortic constriction\u2013induced HF. Furthermore, proteomics revealed that DDX5 is involved in RNA splicing in cardiomyocytes. We found that DDX5 regulated the aberrant splicing of Ca\n              <jats:sup>2+<\/jats:sup>\n              \/calmodulin-dependent protein kinase II\u03b4 (\n              <jats:italic toggle=\"yes\">CamkII\u03b4<\/jats:italic>\n              ), thus preventing the production of CaMKII\u03b4A, which phosphorylates L-type calcium channel by serine residues of Cacna1c, leading to impaired Ca\n              <jats:sup>2+<\/jats:sup>\n              homeostasis. In line with this, we found increased intracellular Ca\n              <jats:sup>2+<\/jats:sup>\n              transients and increased sarcoplasmic reticulum Ca\n              <jats:sup>2+<\/jats:sup>\n              content in DDX5-depleted cardiomyocytes. Using adeno-associated virus serotype 9 knockdown of CaMKII\u03b4A partially rescued the cardiac dysfunction and HF in\n              <jats:italic toggle=\"yes\">Ddx5<\/jats:italic>\n              knockout mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>These findings reveal a role for DDX5 in maintaining calcium homeostasis and cardiac function by regulating alternative splicing in cardiomyocytes, identifying the DDX5 as a potential target for therapeutic intervention in HF.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.123.064774","type":"journal-article","created":{"date-parts":[[2024,7,26]],"date-time":"2024-07-26T09:00:45Z","timestamp":1721984445000},"page":"1121-1139","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":33,"title":["RNA Helicase DDX5 Maintains Cardiac Function by Regulating\n            <i>CamkII\u03b4<\/i>\n            Alternative Splicing"],"prefix":"10.1161","volume":"150","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4797-7671","authenticated-orcid":true,"given":"Kangni","family":"Jia","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine, Ruijin Hospital (K.J., H.C., W.M., L.Z., Z.L., Z.W., H.S., Y.C., H.Z., H.X., L.Y., Z.C., L.L., R.Z., X.Y.), School of Medicine, Shanghai Jiao Tong University, China."},{"name":"Institute of Cardiovascular Diseases (K.J., H.C., W.M., L.Z., Z.L., Z.W., H.S., Y.C., H.Z., H.X., L.Y., Z.C., L.C., R.Z., X.Y.), School of Medicine, Shanghai Jiao Tong University, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-4898-4363","authenticated-orcid":true,"given":"Haomai","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Ruijin Hospital (K.J., H.C., W.M., L.Z., Z.L., Z.W., H.S., Y.C., H.Z., H.X., L.Y., Z.C., L.L., R.Z., X.Y.), School of Medicine, Shanghai Jiao Tong University, China."},{"name":"Institute of Cardiovascular Diseases (K.J., H.C., W.M., L.Z., Z.L., Z.W., H.S., Y.C., H.Z., H.X., L.Y., Z.C., L.C., R.Z., X.Y.), School of Medicine, Shanghai Jiao Tong University, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0287-8496","authenticated-orcid":true,"given":"Wenqi","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Ruijin Hospital (K.J., H.C., W.M., L.Z., Z.L., Z.W., H.S., Y.C., H.Z., H.X., L.Y., Z.C., L.L., R.Z., X.Y.), School of Medicine, Shanghai Jiao Tong University, China."},{"name":"Institute of Cardiovascular Diseases (K.J., H.C., W.M., L.Z., Z.L., Z.W., H.S., Y.C., H.Z., H.X., L.Y., Z.C., L.C., R.Z., X.Y.), School of Medicine, Shanghai Jiao Tong University, 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