ArticleAging2019
Upregulation of miR-93 and inhibition of LIMK1 improve ventricular remodeling and alleviate cardiac dysfunction in rats with chronic heart failure by inhibiting RhoA/ROCK signaling pathway activation.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Crosstalk between microRNA and Oxidative Stress in Heart Failure: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- The microRNA Expression Profiling in Heart Failure: A Systematic Review and Meta-Analysis.Frontiers in cardiovascular medicine · 2022Pooled it
- A meta-analysis of microRNA expression profiling studies in heart failure.Heart failure reviews · 2021Pooled it
- Ginsenoside Rb1 protects hair cell-like HEI-OC1 cells against apoptosis by inhibiting the activation of the Fas system induced by the RhoA/ROCK/LIMK1 pathway.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Endothelial ferroptosis: a novel mechanism and therapeutic target in diabetic microvascular complications.Molecular medicine (Cambridge, Mass.) · 2026Review
- N6-methyladenosine modification of CBLB affects LPS-induced endoplasmic reticulum stress in alveolar epithelial cells.Central-European journal of immunology · 2026Article
- Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner.Cell death & disease · 2025Article
- Heart failure, inflammation and exercise.International journal of biological sciences · 2025Review
- MicroRNA-30a-5p Promotes Chronic Heart Failure in Rats by Targeting Sirtuin-1 to Activate the Nuclear Factor-κB/NOD-Like Receptor 3 Signaling Pathway.Cardiovascular drugs and therapy · 2023Review
- Integrative transcriptomics and cell systems analyses reveal protective pathways controlled by Igfbp-3 in anthracycline-induced cardiotoxicity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- MiR-568 mitigated cardiomyocytes apoptosis, oxidative stress response and cardiac dysfunction via targeting SMURF2 in heart failure rats.Heart and vessels · 2023Article
- 25-hydroxyvitamin D3 inhibits oxidative stress and ferroptosis in retinal microvascular endothelial cells induced by high glucose through down-regulation of miR-93.BMC ophthalmology · 2023Article
- Investigating the Anticancer Activity of G-Rh1 Using In Silico and In Vitro Studies (A549 Lung Cancer Cells).Molecules (Basel, Switzerland) · 2022Article
- LncRNA HOXA11-AS promotes vascular endothelial cell injury in atherosclerosis by regulating the miR-515-5p/ROCK1 axis.ESC heart failure · 2022Article
- Differentially expressed TUG1 and miR-145-5p indicate different severity of chronic heart failure and predict 2-year survival prognosis.Experimental and therapeutic medicine · 2021Article
- Silenced SOX2-OT alleviates ventricular arrhythmia associated with heart failure by inhibiting NLRP3 expression via regulating miR-2355-3p.Immunity, inflammation and disease · 2021Article
- Identification of biomarkers, pathways, and potential therapeutic targets for heart failure using next-generation sequencing data and bioinformatics analysis.Therapeutic advances in cardiovascular diseaseArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThere are some researches about the role of microRNA (miRNA) in chronic heart failure (CHF) were performed, but the study about miR-93's function in CHF is scarcely investigated. Thus, we determined to probe into the effects of miR-93 in rats with CHF by targeting LIMK1 through regulating RhoA/ROCK pathway.
resultsWe found increased LIMK1 and decreased miR-93 in CHF rats, and up-regulation of miR-93 inhibited LIMK1, RhoA and ROCK1 expression in CHF rats. Up-regulation of miR-93 or inhibition of LIMK1 decreased oxidative stress, inflammatory factors, as well as apoptosis-related indicators in CHF rats. LIMK1 was confirmed as a direct target gene of miR-93.
conclusionOur study provides evidence that upregulated miR-93 and downregulated LIMK1 improve ventricular remodeling and reduce cardiac dysfunction in CHF rats by inhibiting RhoA/ROCK signaling pathway activation.
methodsFirst, rat models of CHF were established by aortic coarctation, and the rats were injected with miR-93 mimics, LIMK1-siRNA or overexpressed-LIMK1. Then expression of miR-93, LIMK1, RhoA, and ROCK1 expression in myocardial tissues were detected, after which indices of cardiac ultrasound, hemodynamics, and oxidative stress, inflammatory factors, apoptosis-related indicators were detected via a series of assays. Finally, the targeting relationship of miR-93 and LIMK1 was verified.
Indexed as
Identifiers
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.