ArticleNature communications2020
Macrophage secretion of miR-106b-5p causes renin-dependent hypertension.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Emerging Prognostic Risk Factors in Acute Coronary Syndromes: Beyond Traditional Risk Assessment.Journal of clinical medicine · 2026Review
- Plasma Expression andBiomolecules · 2026Article
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Exosomes in hypertension: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Vitamin D deficiency is associated with elevated blood concentrations of ethylene oxide.BMC public health · 2025Article
- LncRNA IGF2-AS serves as a miR-106b-5p sponge to induce apoptosis and inflammatory reaction of bronchial epithelial cells in COPD.BMC pulmonary medicine · 2025Article
- Current Knowledge of the Impact of Vitamin D in Coronary Artery Disease.International journal of molecular sciences · 2025Review
- The Diagnostic and Predictive Potential of miR-328 in Atrial Fibrillation: Insights from a Spontaneously Hypertensive Rat Model.International journal of molecular sciences · 2025Article
- Identification of an Exosomal miRNA Signature in Newly Diagnosed Essential Hypertensive Adults.British journal of biomedical science · 2025Article
- Mechanisms and Prevention Strategies of Macrophage Involvement in the Progression From Hypertension to Heart Failure.International journal of hypertension · 2025Review
- A roadmap to the molecular human linking multiomics with population traits and diabetes subtypes.Nature communications · 2024Article
- Immune mechanisms in the pathophysiology of hypertension.Nature reviews. Nephrology · 2024Review
- A Systematic Review and Meta-Analysis of microRNA Profiling Studies in Chronic Kidney Diseases.Non-coding RNA · 2024Review
- Endoplasmic reticulum stress-mediated cell death in cardiovascular disease.Cell stress & chaperones · 2024Review
- Vitamin D and Cardiovascular Diseases: An Update.Cureus · 2023Review
- Associations of leptin receptors and miRNA polymorphisms with susceptibility to hypertension.Biomedical reports · 2023Article
- Inhibition of MiR-106b-5p mediated by exosomes mitigates acute kidney injury by modulating transmissible endoplasmic reticulum stress and M1 macrophage polarization.Journal of cellular and molecular medicine · 2023Article
- JMJD3 ablation in myeloid cells confers renoprotection in mice with DOCA/salt-induced hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- The RNA-binding protein LRPPRC promotes resistance to CDK4/6 inhibition in lung cancer.Nature communications · 2023Article
- Genetic associations between miR‑200bT>C and miR‑495A>C polymorphisms and hypertension susceptibility.Experimental and therapeutic medicine · 2023Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
Abstract
Myeloid cells are known mediators of hypertension, but their role in initiating renin-induced hypertension has not been studied. Vitamin D deficiency causes pro-inflammatory macrophage infiltration in metabolic tissues and is linked to renin-mediated hypertension. We tested the hypothesis that impaired vitamin D signaling in macrophages causes hypertension using conditional knockout of the myeloid vitamin D receptor in mice (KODMAC). These mice develop renin-dependent hypertension due to macrophage infiltration of the vasculature and direct activation of renal juxtaglomerular (JG) cell renin production. Induction of endoplasmic reticulum stress in knockout macrophages increases miR-106b-5p secretion, which stimulates JG cell renin production via repression of transcription factors E2f1 and Pde3b. Moreover, in wild-type recipient mice of KODMAC/miR106b
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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.