ArticleCell death discovery2022
METTL3-mediated macrophage exosomal NEAT1 contributes to hepatic fibrosis progression through Sp1/TGF-β1/Smad signaling pathway.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 30 citations in OpenAlex.
- Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Review
- mRedox biology · 2026Review
- Defining the RNA Modification Landscape of Multiple Myeloma Reveals METTL3-Dependent mbioRxiv : the preprint server for biology · 2026Article
- M2 macrophage-derived apoptotic vesicles alleviate liver fibrosis via miR-1224-5p-mediated inhibition of the SP1/TGF-β pathway in hepatic stellate cells.Journal of nanobiotechnology · 2026Article
- Noncoding RNAs: A Novel Frontier in Liver Cancer Research and Therapy: Implications for Precision Oncology.Sub-cellular biochemistry · 2026Review
- Exosomes Regulate Liver Diseases Through the TGF-β1/Smads Signaling Pathway and the Intervention of Traditional Chinese Medicine: A Narrative Review.Journal of inflammation research · 2026Review
- Extracellular Vesicle-Packaged circTAX1BP1 from Cancer-Associated Fibroblasts Regulates RNA m6A Modification through Lactylation of VIRMA in Colorectal Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sympathetic Activation Promotes Kidney Fibrosis in Mice via Macrophage-Derived N2ICD-Enriched Extracellular Vesicles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Mesenchymal stem cell exosomes regulate TGFβ/Smad3 by decreasing the METTL3-NEAT1 axis to inhibit scar progression after breast surgery.Journal of molecular histology · 2025Article
- Exosome-mediated effects of BRCA1 on cardiovascular artery disease.Cell biology and toxicology · 2025Article
- m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs.Briefings in functional genomics · 2025Review
- Article
- The role of RNA modifications in disease-associated macrophages.Molecular therapy. Nucleic acids · 2024Review
- CRISPR/Cas13 sgRNA-Mediated RNA-RNA Interaction Mapping in Live Cells with APOBEC RNA Editing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseases.Clinical epigenetics · 2024Review
- Article
- The effects of intracellular and exosomal ncRNAs on cancer progression.Cancer gene therapy · 2023Review
- Puerarin alleviates chronic renal failure-induced pyroptosis in renal tubular epithelial cells by targeting miR-342-3p/TGF-β/SMAD axis.Genes & genomics · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic fibrosis (HF) is caused by chronic hepatic injury and is characterized by hepatic stellate cells (HSCs) activation. Studies focusing on the function of exosomes derived from macrophages in HF progression are limited. This study aims to identify the roles of exosomal NEAT1 derived from macrophages on HF and the underlying mechanisms. Our studies showed that METTL3 targeted and enhanced NEAT1 expression in macrophages. Exosomal NEAT1 originating from LPS-treated macrophages promoted HSCs proliferation and migration, and induced the expression of fibrotic proteins including collagen I, α-SMA, and fibronectin. Macrophage exosomal NEAT1 contributed to HSCs activation by sponging miR-342. MiR-342 directly targeted Sp1 and suppressed its downstream TGF-β1/Smad signaling pathway, which eventually led to the inhibition of HSCs activation. Depletion of NEAT1 in the macrophage exosomes inhibited HF progression both in vitro and in vivo. Altogether, our study proved that silence of NEAT1 in the macrophage exosomes exerted protective roles against HF through the miR-342/Sp1/TGF-β1/Smad signaling pathway, suggesting a potential therapeutic target in HF treatment.
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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.