ArticleJournal of cardiovascular translational research2025
LncRNA SMILR Serves a Diagnostic Biomarker in Patients with Chronic Heart Failure and Regulates Functions of Vascular Endothelial Cells.
Article in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- BCYRN1 silencing alleviates cardiomyocyte inflammation and apoptosis in chronic heart failure via the miR-455-3p/BAX axis.Molecular and cellular biochemistry · 2026Article
- LncRNA HOXA11-AS Promotes Myocardial Injury in Chronic Heart Failure by Sponging miR-342-3p.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Investigated the role and possible mechanisms of SMILR in angiogenesis among chronic heart failure (CHF) patients to establish novel biomarkers for the clinical assessment of CHF. qPCR was employed to assess the levels of serum SMILR and miR-10b-3p. ROC analysis and logistic regression were utilized to evaluate the diagnostic and predictive value of SMILR. Pearson correlation analysis was conducted to explore the relationship between serum SMILR and myocardial injury markers, as well as cardiac function indicators. In CHF patients, serum SMILR was up-regulated, while miR-10b-3p was down-regulated. In a hypoxic injury model, SMILR silencing restored both the function and oxidative stress levels of hCMECs, and promoted the secretion of pro-angiogenic factors. Inhibition of miR-10b-3p prevented the angiogenic enhancement associated with the knockdown of SMILR. SMILR influences angiogenesis and CHF progression via miR-10b-3p. SMILR is a promising candidate for early detection and subsequent therapy in CHF.
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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 OpenQuestion graph.