{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Han L"],"funding":["American Heart Association","U.S. Department of Health &amp; Human Services | NIH | Office of Extramural Research, National Institutes of Health","NHLBI NIH HHS"],"pagination":["1033-1046"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10344779"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(7)"],"pubmed_abstract":["Lipid droplets (LDs) are cellular organelles critical for lipid homeostasis, with intramyocyte LD accumulation implicated in metabolic disorder-associated heart diseases. Here we identify a human long non-coding RNA, Lipid-Droplet Transporter (LIPTER), essential for LD transport in human cardiomyocytes. LIPTER binds phosphatidic acid and phosphatidylinositol 4-phosphate on LD surface membranes and the MYH10 protein, connecting LDs to the MYH10-ACTIN cytoskeleton and facilitating LD transport. LIPTER and MYH10 deficiencies impair LD trafficking, mitochondrial function and survival of human induced pluripotent stem cell-derived cardiomyocytes. Conditional Myh10 deletion in mouse cardiomyocytes leads to LD accumulation, reduced fatty acid oxidation and compromised cardiac function. We identify NKX2.5 as the primary regulator of cardiomyocyte-specific LIPTER transcription. Notably, LIPTER transgenic expression mitigates cardiac lipotoxicity, preserves cardiac function and alleviates cardiomyopathies in high-fat-diet-fed and Lepr<sup>db/db</sup> mice. Our findings unveil a molecular connector role of LIPTER in intramyocyte LD transport, crucial for lipid metabolism of the human heart, and hold significant clinical implications for treating metabolic syndrome-associated heart diseases."],"journal":["Nature cell biology"],"pubmed_title":["Lipid droplet-associated lncRNA LIPTER preserves cardiac lipid metabolism."],"pmcid":["PMC10344779"],"funding_grant_id":["RO1HL147871","R01 HL147871","RO1HL160856","20EIA35260114","R01 HL160856"],"pubmed_authors":["Sheng Y","Huang D","Yang L","Han L","Lu X","Wang C","Wu S","Wan J","Liu S","Broxmeyer HE"],"additional_accession":[]},"is_claimable":false,"name":"Lipid droplet-associated lncRNA LIPTER preserves cardiac lipid metabolism.","description":"Lipid droplets (LDs) are cellular organelles critical for lipid homeostasis, with intramyocyte LD accumulation implicated in metabolic disorder-associated heart diseases. Here we identify a human long non-coding RNA, Lipid-Droplet Transporter (LIPTER), essential for LD transport in human cardiomyocytes. LIPTER binds phosphatidic acid and phosphatidylinositol 4-phosphate on LD surface membranes and the MYH10 protein, connecting LDs to the MYH10-ACTIN cytoskeleton and facilitating LD transport. LIPTER and MYH10 deficiencies impair LD trafficking, mitochondrial function and survival of human induced pluripotent stem cell-derived cardiomyocytes. Conditional Myh10 deletion in mouse cardiomyocytes leads to LD accumulation, reduced fatty acid oxidation and compromised cardiac function. We identify NKX2.5 as the primary regulator of cardiomyocyte-specific LIPTER transcription. Notably, LIPTER transgenic expression mitigates cardiac lipotoxicity, preserves cardiac function and alleviates cardiomyopathies in high-fat-diet-fed and Lepr<sup>db/db</sup> mice. Our findings unveil a molecular connector role of LIPTER in intramyocyte LD transport, crucial for lipid metabolism of the human heart, and hold significant clinical implications for treating metabolic syndrome-associated heart diseases.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2026-05-29T09:04:47.087Z","creation":"2025-02-19T00:38:26.828Z"},"accession":"S-EPMC10344779","cross_references":{"pubmed":["37264180"],"doi":["10.1038/s41556-023-01162-4"]}}