ArticleMolecular therapy. Nucleic acids2018
The lncRNA Plscr4 Controls Cardiac Hypertrophy by Regulating miR-214.
Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.GeroScience · 2026Review
- Machine learning-based integration identifies a 10-gene predictive signature and its classification patterns in schizophrenia.European archives of psychiatry and clinical neuroscience · 2026Article
- Long non-coding RNA profiling of hypertrophic cardiomyopathy in mice.Scientific data · 2026Article
- Cardiac hypertrophy at the crossroads: Mechanistic insights and emerging multimodal therapeutic strategies.European journal of pharmacology · 2025Review
- Investigating the role of long non-coding RNA in hypertrophic cardiomyopathy.bioRxiv : the preprint server for biology · 2025Article
- Mitochondria-resident SBK3 confers protection against pressure overload-induced heart failure in mice.Acta biochimica et biophysica Sinica · 2025Article
- SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism.Scientific reports · 2025Article
- Advances in pharmacological research on myocardial remodeling agents: A decade in review.Medicine · 2025Review
- The lncRNA Jpx participates in testosterone-induced H9c2 cell hypertrophy by targeting the miR-145-5p/Nfatc3 axis.Frontiers in cell and developmental biology · 2025Article
- lncRNA Gm20257 alleviates pathological cardiac hypertrophy by modulating the PGC-1α-mitochondrial complex IV axis.Frontiers of medicine · 2024Article
- Long non-coding RNAs in cardiac hypertrophy and heart failure: functions, mechanisms and clinical prospects.Nature reviews. Cardiology · 2024Review
- Predictive biomarkers for the early detection and management of heart failure.Heart failure reviews · 2024Review
- Regulatory mechanisms of long non-coding RNAs on mitochondrial function in congestive heart failure.Non-coding RNA research · 2024Review
- Posttranscriptional Regulation by Proteins and Noncoding RNAs.Advances in experimental medicine and biology · 2024Article
- The role and medical prospects of long non-coding RNAs in cardiovascular disease.Heart failure reviews · 2023Review
- Long non-coding RNA KCND1 protects hearts from hypertrophy by targeting YBX1.Cell death & disease · 2023Article
- mRNA, miRNA, lncRNA, ceRNA: The Future of Cardiovascular Research?Arquivos brasileiros de cardiologia · 2023Article
- Non-coding RNAs regulating mitochondrial function in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Impact of Vitamin D Supplementation on the Clinical Outcomes and Epigenetic Markers in Patients with Acute Coronary Syndrome.Pharmaceuticals (Basel, Switzerland) · 2023Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy accompanied by maladaptive cardiac remodeling is the uppermost risk factor for the development of heart failure. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have various biological functions, and their vital role in the regulation of cardiac hypertrophy still needs to be explored. In this study, we demonstrated that lncRNA Plscr4 was upregulated in hypertrophic mice hearts and in angiotensin II (Ang II)-treated cardiomyocytes. Next, we observed that overexpression of Plscr4 attenuated Ang II-induced cardiomyocyte hypertrophy. Conversely, the inhibition of Plscr4 gave rise to cardiomyocyte hypertrophy. Furthermore, overexpression of Plscr4 attenuated TAC (transverse aortic constriction)-induced cardiac hypertrophy. Finally, we demonstrated that Plscr4 acted as an endogenous sponge of miR-214 and forced expression of Plscr4 downregulated miR-214 expression to promote Mfn2 and attenuate hypertrophy. In contrast, knockdown of Plscr4 upregulated miR-214 to induce cardiomyocyte hypertrophy. Additionally, luciferase assay showed that miR-214 was the direct target of Plscr4, and overexpression of miR-214 counteracted the anti-hypertrophy effect of Plscr4. Collectively, these findings identify Plscr4 as a negative regulator of cardiac hypertrophy in vivo and in vitro due to its regulation of the miR-214-Mfn2 axis, suggesting that Plscr4 might act as a therapeutic target for the treatment of cardiac hypertrophy and heart failure.
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