ArticleCell biology and toxicology2022
The aberrant cross-talk of epithelium-macrophages via METTL3-regulated extracellular vesicle miR-93 in smoking-induced emphysema.
Article in Cell biology and toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.
- The Effect of Cigarettes and E-Cigarettes on Epithelial-Derived Extracellular Vesicles: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Extracellular vesicles and chronic obstructive pulmonary disease (COPD): a systematic review.Respiratory research · 2022Pooled it
- RNA modifications in intestinal macrophages: Implications for gut immunity and inflammation.Genes & diseases · 2026Review
- Bronchial epithelial-derived exosomal SLC6A14 promotes airway inflammation and mucus hypersecretion via the ZFP36L1/IL-8 axis.Functional & integrative genomics · 2026Article
- MicroRNA chemical modifications in post-transcriptional gene silencing and human diseases.Molecular therapy. Nucleic acids · 2025Review
- Extracellular Vesicles: Multimodal Tools for Diagnosis, Prognosis, and Therapy in Respiratory Diseases.Expert reviews in molecular medicine · 2025Review
- Article
- FSP1 Acts in Parallel with GPX4 to Inhibit Ferroptosis in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- Extracellular Vesicle microRNA: A Promising Biomarker and Therapeutic Target for Respiratory Diseases.International journal of molecular sciences · 2024Review
- The indispensability of methyltransferase-like 3 in the immune system: from maintaining homeostasis to driving function.Frontiers in immunology · 2024Review
- Advances in Intercellular Communication Mediated by Exosomal ncRNAs in Cardiovascular Disease.International journal of molecular sciences · 2023Review
- Emerging Roles for DNA 6mA and RNA m6A Methylation in Mammalian Genome.International journal of molecular sciences · 2023Review
- The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia.European journal of medical research · 2023Review
- Small RNA modifications: regulatory molecules and potential applications.Journal of hematology & oncology · 2023Review
- N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2.Cell death and differentiation · 2023Article
- Molecular mechanisms of environmental exposures and human disease.Nature reviews. Genetics · 2023Review
- Emerging role of N6-methyladenosine RNA methylation in lung diseases.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- NCOA4-Mediated Ferroptosis in Bronchial Epithelial Cells Promotes Macrophage M2 Polarization in COPD Emphysema.International journal of chronic obstructive pulmonary disease · 2022Article
- Epitranscriptomics of Ischemic Heart Disease-The IHD-EPITRAN Study Design and Objectives.International journal of molecular sciences · 2021Article
- Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure.Frontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Cigarette smoke (CS), a complex chemical indoor air pollutant, induces degradation of elastin, resulting in emphysema. Aberrant cross-talk between macrophages and bronchial epithelial cells is essential for the degradation of elastin that contributes to emphysema, in which extracellular vesicles (EVs) play a critical role. The formation of N6-methyladenosine (m6A) is a modification in miRNA processing, but its role in the development of emphysema remains unclear. Here, we established that production of excess mature microRNA-93 (miR-93) in bronchial epithelial cells via enhanced m6A modification was mediated by overexpressed methyltransferase-like 3 (METTL3) induced by CS. Mature miR-93 was transferred from bronchial epithelial cells into macrophages by EVs. In macrophages, miR-93 activated the JNK pathway by targeting dual-specificity phosphatase 2 (DUSP2), which elevated the levels of matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema. These results demonstrate that METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 may use as a novel risk biomarker for CS-induced emphysema.
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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 Socratic graph.