ArticleNature communications2019
Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis.
Article in Nature communications, 2019. 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 79 papers, 1 of them a synthesis that pooled it.
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
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 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
- Role of miR-155 and miR-103 in Oxidative Stress in Cardiovascular Disease: A Narrative Review.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Review
- Higher Expression of miR-155 and miR-103 in Patients with Gitelman Syndrome: Potential Implications for Angiotensin II-Induced Cardiovascular Remodeling in Hypertension.Kidney & blood pressure research · 2026Article
- Circulating miRNAs in pediatric obesity: a single-center exploratory study of their potential association with renal function.Frontiers in molecular biosciences · 2026Article
- Smooth muscle cell (SMC)-Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death.Biochemistry and biophysics reports · 2025Article
- miR-7213-5p-mediated suppression of CCL19 in fibroblast cells may attenuate lupus nephritis.Clinical and experimental medicine · 2025Article
- Porphyromonas gingivalis infection of oral keratinocytes drives the release of pro-inflammatory extracellular vesicles.Scientific reports · 2025Article
- Diabetes Advances Cardiomyocyte Senescence Through Interfering Rnd3 Expression and Function.Aging cell · 2025Article
- Navigating the Maze of Kinases: CaMK-like Family Protein Kinases and Their Role in Atherosclerosis.International journal of molecular sciences · 2024Review
- A Systematic Review and Meta-Analysis of microRNA Profiling Studies in Chronic Kidney Diseases.Non-coding RNA · 2024Review
- LYC inhibits the AKT signaling pathway to activate autophagy and ameliorate TGFB-induced renal fibrosis.Autophagy · 2024Article
- A Novel Tumor-Associated Neutrophil-Related Risk Signature Based on Single-Cell and Bulk RNA-Sequencing Analyses Predicts the Prognosis and Immune Landscape of Breast Cancer.Journal of Cancer · 2024Article
- Aerobic exercise up-regulates Klotho to improve renal fibrosis associated with aging and its mechanism.PloS one · 2024Article
- Plasma Levels of mir-34a-5p Correlate with Systemic Inflammation and Low Naïve CD4 T Cells in Common Variable Immunodeficiency.Journal of clinical immunology · 2023Article
- Potential Roles of microRNAs for Assessing Cardiovascular Risk in Pre-Eclampsia-Exposed Postpartum Women and Offspring.International journal of molecular sciences · 2023Review
- DNA Damage and Nuclear Morphological Changes in Cardiac Hypertrophy Are Mediated by SNRK Through Actin Depolymerization.Circulation · 2023Article
- STING/ACSL4 axis-dependent ferroptosis and inflammation promote hypertension-associated chronic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Article
- Circulating non-coding RNAs in chronic kidney disease and its complications.Nature reviews. Nephrology · 2023Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Although angiotensin II (AngII) is known to cause renal injury and fibrosis, the underlying mechanisms remain poorly characterized. Here we show that hypertensive nephropathy (HN) patients and AngII-infused mice exhibit elevated levels of circulating miR103a-3p. We observe a positive correlation between miR-103a-3p levels and AngII-induced renal dysfunction. miR-103a-3p suppresses expression of the sucrose non-fermentable-related serine/threonine-protein kinase SNRK in glomerular endothelial cells, and glomeruli of HN patients and AngII-infused mice show reduced endothelial expression of SNRK. We find that SNRK exerts anti-inflammatory effects by interacting with activated nuclear factor-κB (NF-κB)/p65. Overall, we demonstrate that AngII increases circulating miR-103a-3p levels, which reduces SNRK levels in glomerular endothelial cells, resulting in the over-activation of NF-κB/p65 and, consequently, renal inflammation and fibrosis. Together, our work identifies miR-103a-3p/SNRK/NF-κB/p65 as a regulatory axis of AngII-induced renal inflammation and fibrosis.
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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.