ArticlePloS one2015
miR-185 plays an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- A meta-analysis of microRNA expression profiling studies in heart failure.Heart failure reviews · 2021Pooled it
- Plasma Expression andBiomolecules · 2026Article
- What role do miRNAs play in the injured heart of the infertile female?Biochemistry and biophysics reports · 2025Review
- Dual-Omics Mapping of Tinnitus Phenotype Transition in Noise-Exposed Auditory Cortex.Cellular and molecular neurobiology · 2025Article
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- lncRNA-056298 Regulates GAP43 and Promotes Cardiac Intrinsic Autonomic Nerve Remodelling in a Canine Model of Atrial Fibrillation Induction after Ganglionated Plexus Ablation.Current medicinal chemistry · 2025Article
- Next-generation sequencing profiling of miRNAs in individuals with 22q11.2 deletion syndrome revealed altered expression of miR-185-5p.Human genomics · 2024Article
- Understanding the Variability of 22q11.2 Deletion Syndrome: The Role of Epigenetic Factors.Genes · 2024Review
- Apigenin Attenuates Transverse Aortic Constriction-Induced Myocardial Hypertrophy: The Key Role of miR-185-5p/SREBP2-Mediated Autophagy [Letter].Drug design, development and therapy · 2024Article
- FSP1 confers ferroptosis resistance in KEAP1 mutant non-small cell lung carcinoma in NRF2-dependent and -independent manner.Cell death & disease · 2023Article
- Clinical Significance of MicroRNAs, Long Non-Coding RNAs, and CircRNAs in Cardiovascular Diseases.Cells · 2023Review
- MicroRNA profiling of the feline left heart identifies chamber-specific expression signatures in health and in advanced hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2023Article
- Non-coding RNA mediates endoplasmic reticulum stress-induced apoptosis in heart disease.Heliyon · 2023Review
- Coding and Noncoding Genes Involved in Atrophy and Compensatory Muscle Growth in Nile Tilapia.Cells · 2022Article
- LncRNA ROR modulates myocardial ischemia-reperfusion injury mediated by the miR-185-5p/CDK6 axis.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88.Molecular medicine (Cambridge, Mass.) · 2022Article
- Review
- Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction.Internal medicine (Tokyo, Japan) · 2022Article
- Downregulation of microRNA-185 expression in diabetic patients increases the expression of NOS2 and results in vascular injury.Experimental and therapeutic medicine · 2021Article
- Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p.Drug design, development and therapy · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miRNA) is an endogenous non-coding RNA species that either inhibits RNA translation or promotes degradation of target mRNAs. miRNAs often regulate cellular signaling by targeting multiple genes within the pathways. In the present study, using Gene Set Analysis, a useful bioinformatics tool to identify miRNAs with multiple target genes in the same pathways, we identified miR-185 as a key candidate regulator of cardiac hypertrophy. Using a mouse model, we found that miR-185 was significantly down-regulated in myocardial cells during cardiac hypertrophy induced by transverse aortic constriction. To confirm that miR-185 is an anti-hypertrophic miRNA, genetic manipulation studies such as overexpression and knock-down of miR-185 in neonatal rat ventricular myocytes were conducted. The results showed that up-regulation of miR-185 led to anti-hypertrophic effects, while down-regulation led to pro-hypertrophic effects, suggesting that miR-185 has an anti-hypertrophic role in the heart. Our study further identified Camk2d, Ncx1, and Nfatc3 as direct targets of miR-185. The activity of Nuclear Factor of Activated T-cell (NFAT) and calcium/calmodulin-dependent protein kinase II delta (CaMKIIδ) was negatively regulated by miR-185 as assessed by NFAT-luciferase activity and western blotting. The expression of phospho-phospholamban (Thr-17), a marker of CaMKIIδ activity, was also significantly reduced by miR-185. In conclusion, miR-185 effectively blocked cardiac hypertrophy signaling through multiple targets, rendering it a potential drug target for diseases such as heart failure.
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