ArticlePloS one2016
MicroRNA-497 Inhibits Cardiac Hypertrophy by Targeting Sirt4.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 53 citations in OpenAlex.
- Subcellular sirtuin signaling networks: pivotal regulators of cardiovascular homeostasis and remodeling.Journal of molecular histology · 2026Review
- The crosstalk between MicroRNAs and sirtuins: a bit unexpected therapeutic target for cardiovascular diseases.European journal of medical research · 2025Review
- SIRT1: The first key to unlocking the mystery of cardiovascular diseases.Frontiers in pharmacology · 2025Review
- CoClFEBS open bio · 2023Article
- The dysregulation of plasma miR-497/FGF23 axis, and its association with clinical characteristics and major adverse cardiovascular event in female premature acute coronary syndrome patients.Irish journal of medical science · 2023Article
- SIRT4 in ageing.Biogerontology · 2023Review
- MiRNA-29b and miRNA-497 Modulate the Expression of Carboxypeptidase X Member 2, a Candidate Gene Associated with Left Ventricular Hypertrophy.International journal of molecular sciences · 2022Article
- Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases.Basic research in cardiology · 2021Review
- Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis.Open life sciences · 2021Article
- A narrative review of the roles of the miR-15/107 family in heart disease: lessons and prospects for heart disease.Annals of translational medicine · 2021Review
- Review
- Functions of mammalian SIRT4 in cellular metabolism and research progress in human cancer.Oncology letters · 2020Review
- A Roadmap for Fixing the Heart: RNA Regulatory Networks in Cardiac Disease.Molecular therapy. Nucleic acids · 2020Review
- MicroRNA-497/fibroblast growth factor-23 axis, a predictive indictor for decreased major adverse cardiac and cerebral event risk in end-stage renal disease patients who underwent continuous ambulatory peritoneal dialysis.Journal of clinical laboratory analysis · 2020Article
- miR-145 inhibits the proliferation and migration of vascular smooth muscle cells by regulating autophagy.Journal of cellular and molecular medicine · 2020Article
- miR-424-5p regulates cell proliferation and migration of esophageal squamous cell carcinoma by targeting SIRT4.Journal of Cancer · 2020Article
- Downregulation of miR-26b-5p, miR-204-5p, and miR-497-3p Expression Facilitates Exercise-Induced Physiological Cardiac Hypertrophy by Augmenting Autophagy in Rats.Frontiers in genetics · 2020Article
- Mitochondrial Function, Metabolic Regulation, and Human Disease Viewed through the Prism of Sirtuin 4 (SIRT4) Functions.Journal of proteome research · 2019Review
- MiR-195-5p Promotes Cardiomyocyte Hypertrophy by Targeting MFN2 and FBXW7.BioMed research international · 2019Article
- Emerging potential benefits of modulating NADAmerican journal of physiology. Heart and circulatory physiology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to overload pressure of heart. From abundant studies, a conclusion is drawn that many microRNAs (miRNAs) are associated with cardiac hypertrophy and heart failure. To investigate the role of microRNA-497 (miR-497) in myocardial hypertrophy, two models were established in this study from cell level to integral level. Cardiac hypertrophy was induced by using angiotensin Ⅱ (Ang Ⅱ) in vitro and was created by transverse abdominal aortic constriction (TAC) in vivo. There was a significant decrease expression of miR-497 in cardiac hypertrophy models. Moreover, overexpression of miR-497 inhibited myocardial hypertrophy both in vitro and in vivo without heart function variation. In addition, luciferase reporter assays demonstrated that Sirt4 was a direct target gene of miR-497. Taking together, our study indicates that miR-497 modulates cardiac hypertrophy by targeting Sirt4 and may serve as a potential therapeutic substance in the course.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.