ArticleScientific reports2025
Targeting SYK with miR-512-3p provides therapeutic potential in myocardial fibrosis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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.
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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
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Engineered extracellular vesicles for ischemic heart diseases: modification methods, targeted delivery strategies, and multi-modal therapies - A systematic review.Frontiers in cardiovascular medicine · 2026Pooled it
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Authors and funding
11 authors.
Funding
Abstract
Myocardial fibrosis is a key pathological process in cardiovascular diseases. The activation of myocardial fibroblasts has been shown to be regulated by several signalling pathways, including Ang II signalling pathway. This study aimed to investigate the role of SYK (spleen tyrosine kinase) in myocardial fibrosis and explore its upstream regulator targeting SYK expression. In an isoproterenol (ISO)-induced myocardial fibrosis murine model, SYK was highly expressed in activated myocardial fibroblasts and colocalized with α-SMA. In vitro, Ang II stimulation increased the levels of SYK and its phosphorylated form, promoting fibroblast activation and ECM protein secretion. SYK knockdown effectively inhibited fibroblast activation in HL-1 cells. Bioinformatics analysis and functional screening identified a novel modulator, miR-512-3p, which can suppress the expression of SYK. In vitro, miR-512-3p inhibited fibroblast activation by targeting SYK, reducing fibrosis and cell proliferation. In vivo, miR-512-3p treatment significantly improved cardiac function, as shown by increased left ventricular ejection fraction and fractional shortening values. Additionally, miR-512-3p attenuated myocardial remodelling, with reductions in the left ventricular posterior wall diameter and diastolic left ventricular anterior wall diameter. These results provide strong in vivo evidences that miR-512-3p exhibits antifibrotic effects and protects against cardiac dysfunction and remodelling, suggesting a promising therapeutic strategy for treating myocardial fibrosis.
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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 Socratic graph.