ArticleCellular & molecular biology letters2018
MicroRNA-495 inhibits the high glucose-induced inflammation, differentiation and extracellular matrix accumulation of cardiac fibroblasts through downregulation of NOD1.
Article in Cellular & molecular biology letters, 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, 44 citations in OpenAlex.
- Prediction of differentially expressed microRNAs in blood as potential biomarkers for Alzheimer's disease by meta-analysis and adaptive boosting ensemble learning.Alzheimer's research & therapy · 2021Pooled it
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- Effects of remote ischemic preconditioning and/or erythropoietin on lung injury induced by skeletal ischemia reperfusion: role of the NLRP3 inflammasome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025Review
- miR-495 promotes intestinal epithelial cell apoptosis through downregulation of Sphingosine-1-phosphate.Physiological reports · 2024Article
- microRNA and the Post-Transcriptional Response to Oxidative Stress during Neuronal Differentiation: Implications for Neurodevelopmental and Psychiatric Disorders.Life (Basel, Switzerland) · 2024Article
- NOD1: a metabolic modulator.Frontiers in endocrinology · 2024Review
- CHI3L1 promotes myocardial fibrosis via regulating lncRNA TUG1/miR-495-3p/ETS1 axis.Apoptosis : an international journal on programmed cell death · 2023Article
- Circulating microRNAs in young individuals with long-duration type 1 diabetes in comparison with healthy controls.Scientific reports · 2023Article
- Article
- Review
- MAntioxidants (Basel, Switzerland) · 2022Article
- Integrated analysis of miRNA-mRNA interaction in pediatric dilated cardiomyopathy.Pediatric research · 2022Article
- Long non-coding RNA-non-coding RNA activated by DNA damage inhibition suppresses hepatic stellate cell activation via microRNA-495-3p/sphingosine 1-phosphate receptor 3 axis.Bioengineered · 2022Article
- The RNA-Binding Protein ESRP1 Modulates the Expression of RAC1b in Colorectal Cancer Cells.Cancers · 2021Article
- NOD1-Targeted Immunonutrition Approaches: On the Way from Disease to Health.Biomedicines · 2021Review
- The program of renal fibrogenesis is controlled by microRNAs regulating oxidative metabolism.Redox biology · 2021Article
- miR-495 reduces neuronal cell apoptosis and relieves acute spinal cord injury through inhibiting PRDM5.Journal of molecular histology · 2021Article
- hsa-miR-4443 inhibits myocardial fibroblast proliferation by targeting THBS1 to regulate TGF-β1/α-SMA/collagen signaling in atrial fibrillation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- miR-495 targets ROCK1 to inhibit lipopolysaccharides-induced WI-38 cells apoptosis and inflammation.The Kaohsiung journal of medical sciences · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNAs (miRNAs) have physiological and pathophysiological functions that are involved in the regulation of cardiac fibrosis. This study aimed to investigate the effects of miR-495 on high glucose-induced cardiac fibrosis in human cardiac fibroblasts (CFs) and to establish the mechanism underlying these effects.
methodsHuman CFs were transfected with an miR-495 inhibitor or mimic and incubated with high glucose. The levels of NOD1 and miR-495 were then determined via quantitative RT-PCR. Pro-inflammatory cytokine levels, cell differentiation and extracellular matrix accumulation were respectively detected using ELISA, quantitative RT-PCR and western blot assays. The luciferase reporter assay, quantitative RT-PCR and western blot were used to explore whether NOD1 was a target of miR-495. The effects of miR-495 on the NF-κB and TGF-β1/Smad signaling pathways were also detected via western blot.
resultsOur results show that high glucose can significantly increase the expression of NOD1 in a time-dependent manner. Upregulation of miR-495 significantly alleviated the high glucose-induced increases in cell differentiation and collagen accumulation of CFs. Moreover, the bioinformatics analysis predicted that NOD1 was a potential target gene for miR-495. The luciferase reporter assay showed that miR-495 can directly target NOD1. The introduction of miR-495 could significantly inhibit the high glucose-activated NF-κB and TGF-β1/Smad signaling pathways.
conclusionUpregulation of miR-495 ameliorates the high glucose-induced inflammatory, cell differentiation and extracellular matrix accumulation of human CFs by modulating both the NF-κB and TGF-β1/Smad signaling pathways through downregulation of NOD1 expression. These results provide further evidence for the protective effect of miR-495 overexpression in cases of high glucose-induced cardiac fibrosis.
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