ArticleMolecular therapy. Nucleic acids2020
miR-150-Based RNA Interference Attenuates Tubulointerstitial Fibrosis through the SOCS1/JAK/STAT Pathway
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Macrophages in Renal Injury, Repair, Fibrosis Following Acute Kidney Injury and Targeted Therapy.Frontiers in immunology · 2022Pooled it
- Predictive value of miR-151a-3p for the onset of sepsis-induced acute kidney injury and its functional role during disease development.BMC immunology · 2026Article
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Jiawei Danggui Buxue Decoction Reduces Apoptosis and EMT of Renal Interstitial Fibrosis by Regulating JAK2/STAT3 Signaling Pathway.Combinatorial chemistry & high throughput screening · 2026Article
- Non-Coding RNA in Type 2 Diabetes Cardio-Renal Complications and SGLT2 Inhibitor Response.International journal of molecular sciences · 2025Review
- The key role of miR‑378 in kidney diseases (Review).Molecular medicine reports · 2025Review
- Gene therapy and kidney diseases.Molecular therapy. Methods & clinical development · 2024Review
- Role of miRNAs in macrophage-mediated kidney injury.Pediatric nephrology (Berlin, Germany) · 2024Review
- Plasma miR-150-5p in Renal Transplant Recipients with Acute Antibody-Mediated Rejection.Journal of clinical medicine · 2024Article
- Macrophages polarization in renal inflammation and fibrosis animal models (Review).Molecular medicine reports · 2024Review
- Lymphocyte-Specific Protein Tyrosine Kinase Contributes to Spontaneous Regression of Liver Fibrosis may by Interacting with Suppressor of Cytokine Signaling 1.Inflammation · 2023Article
- The Role of miRNA in Renal Fibrosis Leading to Chronic Kidney Disease.Biomedicines · 2023Review
- Evolving cognition of the JAK-STAT signaling pathway: autoimmune disorders and cancer.Signal transduction and targeted therapy · 2023Review
- Role of SUMOylation of STAT1 in tubular epithelial‑mesenchymal transition induced by high glucose.Molecular medicine reports · 2023Article
- Crosstalk between proximal tubular epithelial cells and other interstitial cells in tubulointerstitial fibrosis after renal injury.Frontiers in endocrinology · 2023Review
- JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023Review
- Deletion of miR-150 Prevents Spontaneous T Cell Proliferation and the Development of Colitis.Gastro hep advances · 2023Article
- IL-18 deficiency ameliorates the progression from AKI to CKD.Cell death & disease · 2022Article
- Direct and indirect effects of IFN-α2b in malignancy treatment: not only an archer but also an arrow.Biomarker research · 2022Review
- Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated whether microRNA-150 (miR-150)-based RNA interference (RNAi) ameliorates tubular injury and tubulointerstitial fibrosis. Mice injected with folic acid developed tubulointerstitial fibrosis at day 30. miR-150 levels were increased at day 7 and peaked at day 30. At day 30, protein levels of α-smooth muscle actin, fibronectin (FN), and collagen 1 (COL-1) were increased, while suppressor of cytokine signal 1 (SOCS1) was decreased. Kidneys manifested increased macrophage numbers and increased expression of potential mediators: interferon-γ, interleukin-6, and tumor necrosis factor-α. Locked nucleic acid-anti-miR-150, started prior to or after tubular injury and administered twice weekly for 4 weeks, reversed renal inflammation and fibrosis. In HK-2 cells, co-culture with macrophages increased miR-150 expression and decreased SOCS1. Janus kinase (JAK) and signal transducer and activators of transcription (STAT) pathway-related proteins p-JAK1, p-JAK2, p-STAT1, p-STAT3, and pro-fibrotic genes encoding α-smooth muscle actin, FN, and COL-1 were all upregulated. The miR-150 antagonist reversed these transcriptional changes. Lastly, in renal biopsies from patients with chronic interstitial fibrosis, renal miR-150, and pro-fibrotic gene expression and macrophage numbers were increased, while SOCS1 expression was decreased. In conclusion, miR-150-based RNAi is as a potential novel therapeutic agent for tubulointerstitial fibrosis, suppressing the SOCS1/JAK/STAT pathway and reducing macrophage influx.
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