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Coding potential was verified by bioinformatic and biologic assays. Recombinant adeno-associated virus with cardiac-specific promoter was used to deliver lncRNA in vivo, while cardiac structure and functions were assessed by echocardiography and catheter. Sarcomere shortening, calcium imaging, gene expression profiling, and pull-down assays were performed to investigate the underlying mechanisms. ZNF593-AS, which mainly localized in the cytoplasm of cardiomyocytes, was robustly decreased in the failing heart of patients with DCM, as well as in phenylephrine-treated human cardiomyocytes. Overexpression of mmu-ZNF593-AS significantly improved transverse aortic constriction-induced cardiac dysfunction in mice. Moreover, ZNF593-AS overexpression restored the aberrant Ca\n              <jats:sup>2+<\/jats:sup>\n              handling and contractility of cardiomyocytes from transverse aortic constriction-treated mice. Furthermore, we found that ZNF593-AS acted as a guide RNA scaffold and recruited HNRNPC (heterogeneous nuclear ribonucleoprotein C [C1\/C2]) to RYR2 (ryanodine receptor type 2) mRNA, which, in turn, facilitated RYR2 mRNA stability, contributed to the improvement of cardiac Ca\n              <jats:sup>2+<\/jats:sup>\n              handling and contractile function in DCM.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>Our findings suggested that lncRNA-based therapeutics may protect against DCM.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.120.318437","type":"journal-article","created":{"date-parts":[[2021,2,8]],"date-time":"2021-02-08T22:33:13Z","timestamp":1612823593000},"page":"1708-1723","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":49,"title":["LncRNA ZNF593-AS Alleviates Contractile Dysfunction in Dilated 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