ArticleScientific reports2018
MiR-26a-5p regulates cardiac fibroblasts collagen expression by targeting ULK1.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Cardiovascular System is Influenced by Skeletal Muscle-derived Extracellular Vesicles, Myokines and MicroRNAs Based on Interorgan Communication: A Systematic Review.International journal of medical sciences · 2025Pooled it
- Mapping the miRNA landscape of primitive macrophage extracellular vesicles highlights their pro-vasculogenic effects in engineered human cardiac tissue.APL bioengineering · 2026Article
- Deciphering lncRNA and circRNA control of autophagy in osteosarcoma mechanisms and clinical translation.Discover oncology · 2026Review
- Review
- Cardiac Left Ventricular miRNA-26a Is Downregulated in Ovariectomized Mice, Upregulated upon 17-Beta Estradiol Replacement, and Inversely Correlated with Collagen Type 1 Gene Expression.International journal of molecular sciences · 2024Article
- PDGF-BB accelerates TSCC via fibroblast lactates limiting miR-26a-5p and boosting mitophagy.Cancer cell international · 2024Article
- Autophagy and beyond: Unraveling the complexity of UNC-51-like kinase 1 (ULK1) from biological functions to therapeutic implications.Acta pharmaceutica Sinica. B · 2022Review
- Cardiovascular Disease-Associated MicroRNAs as Novel Biomarkers of First-Trimester Screening for Gestational Diabetes Mellitus in the Absence of Other Pregnancy-Related Complications.International journal of molecular sciences · 2022Article
- New Insights into the Functions of MicroRNAs in Cardiac Fibrosis: From Mechanisms to Therapeutic Strategies.Genes · 2022Review
- LncRNA XIST Prevents Tendon Adhesion and Promotes Tendon Repair Through the miR-26a-5p/COX2 Pathway.Molecular biotechnology · 2022Article
- Current Knowledge of MicroRNAs (miRNAs) in Acute Coronary Syndrome (ACS): ST-Elevation Myocardial Infarction (STEMI).Life (Basel, Switzerland) · 2021Review
- Upregulation of miR‑128 inhibits neuronal cell apoptosis following spinal cord injury via FasL downregulation by repressing ULK1.Molecular medicine reports · 2021Article
- MicroRNAs as the critical regulators of cisplatin resistance in gastric tumor cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Review
- Autophagy in cardiovascular diseases: role of noncoding RNAs.Molecular therapy. Nucleic acids · 2021Review
- MiRNA-1202 promotes the TGF-β1-induced proliferation, differentiation and collagen production of cardiac fibroblasts by targeting nNOS.PloS one · 2021Article
- Combination of Metformin, Sodium Oxamate and Doxorubicin Induces Apoptosis and Autophagy in Colorectal Cancer CellsFrontiers in oncology · 2021Article
- MicroRNA-26a Protects the Heart Against Hypertension-Induced Myocardial Fibrosis.Journal of the American Heart Association · 2020Article
- Article
- The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy.Cells · 2020Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MiRNA is a class of small non-coding RNA which has an important effect on posttranscriptional gene regulation. It can regulate the expression of the target gene at the mRNA level and further influence the protein level of the target gene. We found that ULK1 may be the target gene of miR-26a-5p, and ULK1 (unc-51 like autophagy activating kinase 1) is a key component in autophagy pathway. In this study, we overexpressed miR-26a-5p by transfecting miR-26a-5p mimic into cells and simultaneously inhibited miR-26a-5p by transfecting miR-26a-5p inhibitor into cells. We demonstrated that overexpression of miR-26a-5p can reduce the expression of ULK1 and collagen I, and decrease the activation of LC3-I to LC3-II. In contrast, inhibition of miR-26a-5p can increase the expression of ULK1 and collagen I, and increase the activation of LC3-I to LC3-II. The Dual-luciferase reporter assay showed that miR-26a-5p directly acted on the 3'UTR of ULK1 and thus affected the expression of ULK1. As such, our study demonstrated that miR-26a-5p might regulate the autophagy in cardiac fibroblasts by targeting ULK1, which may have an effect on cardiac fibrosis. To our knowledge, this is the first study that shows miR-26a-5p regulates the autophagic pathway in cardiac fibroblasts.
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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.