ArticleMolecular medicine reports2021
Inhibiting miR‑1 attenuates pulmonary arterial hypertension in rats.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis 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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Pooled it
- Evaluation of LCN2 and miR-8078 as diagnostic biomarkers for congenital heart disease-associated pulmonary arterial hypertension.ESC heart failure · 2026Article
- CircRNA-based AntimiR therapy: A novel approach to hypertension treatment.Non-coding RNA research · 2025Review
- Plasma miR-1-3p levels predict severity in hospitalized COVID-19 patients.British journal of pharmacology · 2025Article
- Notoginsenoside R1 Improved Hypoxic Pulmonary Hypertension by Inhibiting Glycolysis-Mediated Pulmonary Arterial Vascular Remodeling.Canadian respiratory journal · 2025Article
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
- Comprehensive Insights into Mechanisms for Ventricular Remodeling in Right Heart Failure.Reviews in cardiovascular medicine · 2024Review
- Tongxinluo Activates PI3K/AKT Signaling Pathway to Inhibit Endothelial Mesenchymal Transition and Attenuate Myocardial Fibrosis after Ischemia-Reperfusion in Mice.Chinese journal of integrative medicine · 2024Article
- Blockage of the adenosine APurinergic signalling · 2024Article
- Mechanism of action of non-coding RNAs and traditional Chinese medicine in myocardial fibrosis: Focus on the TGF-β/Smad signaling pathway.Frontiers in pharmacology · 2023Review
- Comprehensive investigation and regulatory function of lncRNAs engaged in western honey bee larval immune response toFrontiers in physiology · 2022Article
- MicroRNA-325-3p Targets Human Epididymis Protein 4 to Relieve Right Ventricular Fibrosis in Rats with Pulmonary Arterial Hypertension.Cardiovascular therapeutics · 2022Article
- New Insights into Pulmonary Hypertension: A Role for Connexin-Mediated Signalling.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRs) are reported to serve key roles in pulmonary arterial hypertension (PAH). miR‑1 has been found in cardiovascular diseases. The present study aimed to determine whether the knockdown of miR‑1 could inhibit right ventricle (RV) remodeling and thereby control PAH in model rats. PAH model rats were established by exposing rats to hypoxia, while cardiac fibroblasts (CFs) obtained from PAH model rats were treated with hypoxia to establish an in vitro model, and RV remodeling was evaluated by Masson staining and the levels of collagen I, collagen III, α‑smooth muscle actin (α‑SMA) and connective tissue growth factor (CTGF) evaluated by western blotting or reverse transcription‑quantitative PCR. The results revealed that the expression levels of miR‑1 were upregulated in the RV of PAH model rats induced with hypoxia and in the CFs treated with hypoxia. The mean pulmonary arterial pressure, RV systolic pressure, RV/(left ventricle + interventricular septum) and RV/tibia length were increased in PAH rats; however, the increases in all parameters were subsequently reversed by transfection with a miR‑1 antagomiR in PAH model rats. The transfection with the miR‑1 antagomiR inhibited the development of RV fibrosis and downregulated the mRNA expression levels of collagen I, collagen III, α‑SMA and CTGF in the RV tissue of PAH model rats. The upregulation of collagen I, collagen III, α‑SMA and CTGF expression levels in hypoxia‑treated CFs was also subsequently reversed by miR‑1 antagomiR transfection. The expression levels of collagen I, collagen III, α‑SMA and CTGF were also upregulated in the CFs obtained from PAH model rats, and these increases were attenuated by miR‑1 antagomiR transfection. The expression levels of phosphorylated (p)‑PI3K and p‑AKT were also upregulated in hypoxia‑treated CFs, and these increases were also inhibited by transfection with miR‑1 antagomiR. In conclusion, these results indicated that inhibiting miR‑1 may attenuate RV hypertrophy and fibrosis in PAH model rats, a mechanism that may involve the PI3K/AKT signaling pathway.
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.