ArticleNature communications2023
The lncRNA Sweetheart regulates compensatory cardiac hypertrophy after myocardial injury in murine males.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 9 citations in OpenAlex.
- Extracellular Vesicles Modulation by an Adiponectin Receptor Agonist Provides Cardioprotection for Myocardial Ischemic Injury.Advanced healthcare materials · 2026Article
- Strain-based characterization of atrioventricular and left atrial remodelling in rat models of heart failure with preserved ejection fraction.Experimental physiology · 2026Article
- LncRNA PVT1 in human cancers: genomic complexity, isoforms, functional elements, mechanism of action, subcellular localization and possible role as a therapeutic target.Molecular cancer · 2026Review
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- LncRNA HSCHARME is altered in human cardiomyopathies and promotes stem cell-derived cardiomyogenesis via splicing regulation.Nature communications · 2025Article
- Salidroside protects against myocardial infarction via activating MIF-mediated mitochondrial quality control.Chinese medicine · 2025Article
- Mef2c- and Nkx2-5-Divergent Transcriptional Regulation of Chick WT1_76127 and Mouse Gm14014 lncRNAs and Their Implication in Epicardial Cell Migration.International journal of molecular sciences · 2024Article
- Expression patterns of housekeeping genes and tissue-specific genes in black goats across multiple tissues.Scientific reports · 2024Article
- Decreased lncRNA HNF4A-AS1 facilitates resistance to sorafenib-induced ferroptosis of hepatocellular carcinoma by reprogramming lipid metabolism.Theranostics · 2024Article
- TheNon-coding RNA · 2023Article
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After myocardial infarction in the adult heart the remaining, non-infarcted tissue adapts to compensate the loss of functional tissue. This adaptation requires changes in gene expression networks, which are mostly controlled by transcription regulating proteins. Long non-coding transcripts (lncRNAs) are taking part in fine-tuning such gene programs. We describe and characterize the cardiomyocyte specific lncRNA Sweetheart RNA (Swhtr), an approximately 10 kb long transcript divergently expressed from the cardiac core transcription factor coding gene Nkx2-5. We show that Swhtr is dispensable for normal heart development and function but becomes essential for the tissue adaptation process after myocardial infarction in murine males. Re-expressing Swhtr from an exogenous locus rescues the Swhtr null phenotype. Genes that depend on Swhtr after cardiac stress are significantly occupied and therefore most likely regulated by NKX2-5. The Swhtr transcript interacts with NKX2-5 and disperses upon hypoxic stress in cardiomyocytes, indicating an auxiliary role of Swhtr for NKX2-5 function in tissue adaptation after myocardial injury.
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