ArticleBMC genomic data2021
Transcriptome signature of miRNA-26b KO mouse model suggests novel targets.
Article in BMC genomic data, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 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
8 citing papers in PubMed, 14 citations in OpenAlex.
- miRNA-26b Is Associated with Increased Connexin-40 Expression in Endothelial Cells Under Flow Conditions.International journal of molecular sciences · 2026Article
- Nonhematopoietic MicroRNA-26bArteriosclerosis, thrombosis, and vascular biology · 2026Article
- MicroRNA-26b-/- augments atherosclerosis, while mimic-loaded nanoparticles reduce atherogenesis.Cardiovascular research · 2025Article
- The loss of microRNA-26b promotes aortic calcification through the regulation of cell-specific target genes.Cardiovascular research · 2025Article
- Article
- miR-26 Deficiency Causes Alterations in Lens Transcriptome and Results in Adult-Onset Cataract.Investigative ophthalmology & visual science · 2024Article
- MicroRNA-26b Attenuates Platelet Adhesion and Aggregation in Mice.Biomedicines · 2022Article
- Correction to: Transcriptome signature of miRNA-26b KO mouse model suggests novel targets.BMC genomic data · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundMicroRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. One of the miRNAs that has been shown to play a role in various pathologies like cancer, neurological disorders and cardiovascular diseases is miRNA-26b. However, these studies only demonstrated rather ambiguous associations without revealing a causal relationship. Therefore, the aim of this study is to establish and validate a mouse model which enables the elucidation of the exact role of miRNA-26b in various pathologies.
resultsA miRNA-26b-deficient mouse model was established using homologous recombination and validated using PCR. miRNA-26b-deficient mice did not show any physiological abnormalities and no effects on systemic lipid levels, blood parameters or tissue leukocytes. Using next generation sequencing, the gene expression patterns in miRNA-26b-deficient mice were analyzed and compared to wild type controls. This supported the already suggested role of miRNA-26b in cancer and neurological processes, but also revealed novel associations of miRNA-26b with thermogenesis and allergic reactions. In addition, detailed analysis identified several genes that seem to be highly regulated by miRNA-26b, which are linked to the same pathological conditions, further confirming the role of miRNA-26b in these pathologies and providing a strong validation of our mouse model.
conclusionsmiRNA-26b plays an important role in various pathologies, although causal relationships still have to be established. The described mouse model of miRNA-26b deficiency is a crucial first step towards the identification of the exact role of miRNA-26b in various diseases that could identify miRNA-26b as a promising novel diagnostic or even therapeutic target in a broad range of pathologies.
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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.