ArticleJournal of cellular and molecular medicine2017
miR-181a and miR-150 regulate dendritic cell immune inflammatory responses and cardiomyocyte apoptosis via targeting JAK1-STAT1/c-Fos pathway.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- miR-150-5p at the Interface of Cancer Biology and Immune Regulation: Dual Roles, Mechanisms, and Therapeutic Opportunities.Journal of Cancer · 2026Review
- Platelet Membrane and miR-181a-5p Doubly Optimized Nanovesicles Enhance Cardiac Repair Post-Myocardial Infarction through Macrophage Polarization.ACS applied materials & interfaces · 2025Article
- Heart failure, inflammation and exercise.International journal of biological sciences · 2025Review
- Nanoparticle-based drug delivery systems targeting inflammatory immune mechanisms in acute myocardial infarction: current advances and perspectives.Frontiers in cardiovascular medicine · 2025Review
- FOS as a biomarker for myocardial infarction treatment with Deng's Yangxin Decoction: a systems biology-based analysis.Frontiers in cardiovascular medicine · 2025Article
- Effect of Mechanical Environment Alterations in 3D Stem Cell Culture on the Therapeutic Potential of Extracellular Vesicles.Biomaterials research · 2025Article
- Review
- Recent Insights into Endogenous Mammalian Cardiac Regeneration Post-Myocardial Infarction.International journal of molecular sciences · 2024Review
- Emerging opportunities to target inflammation: myocardial infarction and type 2 diabetes.Cardiovascular research · 2024Review
- Review
- Key subdomains of mesencephalic astrocyte-derived neurotrophic factor attenuate myocardial ischemia/reperfusion injury by JAK1/STAT1/NF-κB signaling pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- Ssc-miR-101-3p inhibits hypoxia-induced apoptosis and inflammatory response in alveolar type-II epithelial cells of Tibetan pigs via targeting FOXO3.Scientific reports · 2024Article
- Immune cells drive new immunomodulatory therapies for myocardial infarction: From basic to clinical translation.Frontiers in immunology · 2023Review
- UnveilingJournal of inflammation research · 2023Article
- Role of immune cell infiltration and small molecule drugs in adhesive capsulitis: Novel exploration based on bioinformatics analyses.Frontiers in immunology · 2023Article
- Global Characteristics and Dynamics of Single Immune Cells After Myocardial Infarction.Journal of the American Heart Association · 2022Article
- RALY regulate the proliferation and expression of immune/inflammatory response genes via alternative splicing of FOS.Genes and immunity · 2022Article
- MicroRNA-150 (miR-150) and Diabetic Retinopathy: Is miR-150 Only a Biomarker or Does It Contribute to Disease Progression?International journal of molecular sciences · 2022Review
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune inflammatory response plays a crucial role in many cardiac pathophysiological processes, including ischaemic cardiac injury and the post-infarction repair process. MicroRNAs (miRNAs) regulate the development and function of dendritic cells (DCs), which are key players in the initiation and regulation of immune responses; however, the underlying regulatory mechanisms remain unclear. Here, we used the supernatants of necrotic primary cardiomyocytes (Necrotic-S) to mimic the myocardial infarction (MI) microenvironment to investigate the role of miRNAs in the regulation of DC-mediated inflammatory responses. Our results showed that Necrotic-S up-regulated the DC maturation markers CD40, CD83 and CD86 and increased the production of inflammatory cytokines, concomitant with the up-regulation of miR-181a and down-regulation of miR-150. Necrotic-S stimulation activated the JAK/STAT pathway and promoted the nuclear translocation of c-Fos and NF-κB p65, and silencing of STAT1 or c-Fos suppressed Necrotic-S-induced DC maturation and inflammatory cytokine production. The effects of Necrotic-S on DC maturation and inflammatory responses, its activation of the JAK/STAT pathway and the induction of cardiomyocyte apoptosis under conditions of hypoxia were suppressed by miR-181a or miR-150 overexpression. Taken together, these data indicate that miR-181a and miR-150 attenuate DC immune inflammatory responses via JAK1-STAT1/c-Fos signalling and protect cardiomyocytes from cell death under conditions of hypoxia.
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.