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Pathological cardiac hypertrophy is an independent risk factor for the development of heart failure. Long noncoding RNAs (lncRNAs), an emerging class of non-protein-coding transcripts, are involved in regulation of multiple cardiac diseases through diverse molecular mechanism, whereas the role of cytoplasmic lncRNAs in regulating cardiac hypertrophy remains unclear. In this study, we identified a novel and functional long noncoding RNA Gm17501, which was predominantly expressed in the cytoplasm of cardiomyocytes. The expression level of lncRNA Gm17501 was altered in cardiac hypertrophy induced by pressure overload and phenylephrine treatment. Moreover, lncRNA Gm17501 expression was decreased in the heart tissue of patients with heart failure. Silencing lncRNA Gm17501 aggravated cardiac hypertrophy under pathological stress. Inhibition of lncRNA Gm17501 did not alter the expression of nearby genes but decreased mRNA level of calcium handling proteins which were involved in cardiac contraction. Therefore, the cytoplasmic lncRNA Gm17501 might protect cardiomyocytes against hypertrophy, possibly by maintaining calcium signaling pathway.
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http://dx.doi.org/10.1016/j.yexcr.2022.113262 | DOI Listing |
JCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
View Article and Find Full Text PDFRadiology
September 2025
Department of Magnetic Resonance Imaging, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Background MRI-derived arrhythmogenic substrate, including late gadolinium enhancement (LGE) and extracellular volume fraction (ECV), is indicative of sudden cardiac death (SCD) risk in nonischemic dilated cardiomyopathy (DCM). The relative prognostic value of LGE and ECV remains unclear. Purpose To evaluate the performance of LGE and T1 mapping in predicting SCD in patients with DCM and to explore clinical implementation.
View Article and Find Full Text PDFCardiol Rev
September 2025
Departments of Medicine and Cardiology, Westchester Medical Center and New York Medical College, Valhalla, NY.
Heart failure (HF) is a complex clinical syndrome marked by impaired contractility, adverse remodeling, and dysregulated intracellular signaling. Protein kinases are central regulators of cardiac function, modulating calcium handling, gene transcription, hypertrophy, and apoptosis through phosphorylation of target proteins. In HF, chronic activation of kinases such as protein kinase A, protein kinase C, calcium/calmodulin-dependent kinase II, mitogen-activated protein kinases, protein kinase B, and Rho-associated protein kinase contributes to progressive cardiac dysfunction.
View Article and Find Full Text PDFJ Cardiovasc Pharmacol
September 2025
Graduate School of Cardiology, Bengbu Medical University, Bengbu 233000, Anhui, China.
Chronic stress-induced cardiac hypertrophy remains a critical precursor to heart failure, with current therapies limited by incomplete mechanistic targeting. Cyclin-dependent kinases (CDKs), pivotal regulators of cell cycle and stress signaling, are emerging therapeutic targets in cardiovascular pathologies. Using bioinformatics analysis of human hypertrophic cardiomyopathy datasets (GSE5500, GSE136308) and a murine transverse aortic constriction (TAC) model, we investigated the therapeutic effects of the CDK inhibitor R547 (10 mg/kg, intraperitoneal every 3 days) on pressure overload-induced cardiac remodeling.
View Article and Find Full Text PDFMedicine (Baltimore)
September 2025
Department of Nephrology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
The purpose of this article was to study the distribution of left ventricular hypertrophy (LVH) and cardiac valve calcification (CVC), relevant factors, and the relationship of LVH and CVC with survival in maintenance hemodialysis (MHD) patients. A total of 281 MHD patients were included in this retrospective and follow-up study. Echocardiography measurements were performed to evaluate the left ventricular structure and cardiac valve.
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