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Syntabulin (SYBU), known for its role as a motor linker at the outer mitochondrial membrane in neuronal system, has recently been suggested as a HF-associated gene. However, the role of SYBU in regulating cardiac function remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Pressure overload\u2013induced cardiac hypertrophy and HF was produced by transverse aortic constriction in mice and phenylephrine (PE) stimulation in neonatal rat ventricular myocytes. SYBU expression was significantly increased in hypertrophic mouse hearts and patient hearts with dilated cardiomyopathy. The cardiac-specific upregulating SYBU expression, achieved via recombinant adeno-associated virus driven by cardiac troponin T promoter, led to increased cardiomyocyte death and worsened HF under hypertrophic conditions. In contrast, SYBU knockdown mitigated PE-induced cardiomyocyte injury. Structured illumination microscopy and analysis of mitochondria-associated endoplasmic reticulum membrane fractions revealed that SYBU localizes to ER\u2013mitochondria contact sites. SYBU enhances sarcoplasmic reticulum (SR)\u2013mitochondria tethering through interactions with Ryanodine receptor 2 and sarcoplasmic\/endoplasmic reticulum Ca2+-ATPase, leading to mitochondrial Ca2+ overload and impaired mitochondrial respiratory capacity. Furthermore, excessive mitochondrial Ca2+ triggered ER stress and protein kinase A activation, inducing phosphorylation of dynamin-related protein 1 at Ser637, and ultimately disrupting mitochondrial fission and mitophagy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings established a critical role of SYBU in promoting HF by inducing cardiomyocyte injury via increasing SR\u2013mitochondria tethering and impairing mitochondrial fission and mitophagy. Therefore, targeting SYBU and its downstream signalling pathways could be a promising therapeutic strategy to restrain HF in pressure overload\u2013induced cardiac hypertrophy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvag139","type":"journal-article","created":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T07:09:47Z","timestamp":1782716987000},"page":"1642-1659","source":"Crossref","is-referenced-by-count":1,"title":["Syntabulin promotes heart failure by enhancing SR\u2013mitochondria tethering and impairing mitofission"],"prefix":"10.1093","volume":"122","author":[{"given":"Ying","family":"Li","sequence":"first","affiliation":[{"name":"Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Grant Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Shenzhen University Medical School , Shenzhen 518055 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Metabolism and Cardiovascular Homeostasis, Grant Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Shenzhen University Medical School , Shenzhen 518055 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenglin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Grant Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Shenzhen University Medical School , Shenzhen 518055 ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wanwen","family":"Cheng","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Grant Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Shenzhen University Medical School , Shenzhen 518055 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