ArticleTobacco induced diseases2020
PRMT6 mediates inflammation via activation of the NF-κB/p65 pathway on a cigarette smoke extract-induced murine emphysema model.
Article in Tobacco induced diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
12 citing papers in PubMed, 21 citations in OpenAlex.
- Formononetin Alleviates Cigarette Smoke Extract-Induced Lung Injury in Mice with Gut Microbiota and Taurine/SLC6A6/NF-κB Modulation.Molecules (Basel, Switzerland) · 2026Article
- Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.EXCLI journal · 2024Review
- Epigenetic regulation of macrophage activation in chronic obstructive pulmonary disease.Frontiers in immunology · 2024Review
- PU.1 alleviates the inhibitory effects of cigarette smoke on endothelial progenitor cell function and lung-homing through Wnt/β-catenin and CXCL12/CXCR4 pathways.Tobacco induced diseases · 2024Article
- CAPN5 attenuates cigarette smoke extract-induced apoptosis and inflammation in BEAS-2B cells.Tobacco induced diseases · 2024Article
- Relationship Between ACSL4-Mediated Ferroptosis and Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
- The arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD.Nature communications · 2022Article
- Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?International journal of molecular sciences · 2022Review
- Effect of pirfenidone protecting against cigarette smoke extract induced apoptosis.Tobacco induced diseases · 2022Article
- Palmitic acid methyl ester inhibits cardiac arrest-induced neuroinflammation and mitochondrial dysfunction.Prostaglandins, leukotrienes, and essential fatty acids · 2021Article
- Article
- F-Box Protein FBXW17-Mediated Proteasomal Degradation of Protein Methyltransferase PRMT6 Exaggerates CSE-Induced Lung Epithelial Inflammation and Apoptosis.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSmoke-driven lung inflammation is considered to be the major pathophysiology mechanism of Chronic Obstructive Pulmonary Disease (COPD)/emphysema. Protein arginine methyltransferase 6 (PRMT6) is a key epigenetic enzyme, which is related to protecting the tri-methylation of H3K4 (H3K4me3). We hypothesized that PTMT6 protects lung inflammation through the nuclear factor kappa B (NF-κB) pathway.
methodsMice were injected with cigarette smoke extract (CSE) or PBS to establish a mice model, intratracheally instilled with overexpressed PRMT6 or negative control vector. Morphometry of lung slides and lung function were measured. We determined the protein expression of PRMT6 and its related histone targets, the activation of NF-κB pathway, the level of tumor necrosis factor α (TNFα) and interleukin-1β (IL-1β).
resultsAfter PRMT6 overexpression, the morphometry indexes and lung function were improved. Also, the expression of H3K4me3 was decreased. Overexpressed PRMT6 could suppress CSE-induced NF-κB activation and pro-inflammation genes expression.
conclusionsThe overexpressed PRMT6 could serve as an inflammation inhibitor, potentially through blocking the NF-κB/p65 pathway in the murine emphysema model.
Indexed as
Identifiers
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.