ReviewClinical reviews in allergy & immunology2013
Epigenetics in immune-mediated pulmonary diseases.
Review in Clinical reviews in allergy & immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Fibrotic interstitial lung diseases and air pollution: a systematic literature review.European respiratory review : an official journal of the European Respiratory Society · 2020Pooled it
- Review
- Bicyclol attenuates pulmonary fibrosis with silicosis via both canonical and non-canonical TGF-β1 signaling pathways.Journal of translational medicine · 2024Article
- Study on the mechanism of PM2.5 affecting Th1/Th2 immune imbalance through the notch signaling pathway in asthmatic mice.Toxicology research · 2023Article
- Protein arginine N-methyltransferase 4 (PRMT4) contributes to lymphopenia in experimental sepsis.Thorax · 2023Article
- Gene Expression Profiles of the Immuno-Transcriptome in Equine Asthma.Animals : an open access journal from MDPI · 2022Article
- Epigenetic underpinnings of inflammation: Connecting the dots between pulmonary diseases, lung cancer and COVID-19.Seminars in cancer biology · 2022Review
- Epigenetic regulation of inflammation by microRNAs in post-infectious bronchiolitis obliterans.Clinical & translational immunology · 2022Article
- MiR-146a and miR-155 polymorphisms in Egyptian patients with Behcet's disease.Archives of medical science : AMS · 2022Article
- MicroRNA-205-5p targets E2F1 to promote autophagy and inhibit pulmonary fibrosis in silicosis through impairing SKP2-mediated Beclin1 ubiquitination.Journal of cellular and molecular medicine · 2021Article
- Increased Expression of PPAR-γ Modulates Monocytes Into a M2-Like Phenotype in SLE Patients: An Implicative Protective Mechanism and Potential Therapeutic Strategy of Systemic Lupus Erythematosus.Frontiers in immunology · 2020Article
- Fibroblast-to-myofibroblast transition in bronchial asthma.Cellular and molecular life sciences : CMLS · 2018Review
- Genetic Resistance toFrontiers in immunology · 2018Review
- Approaches to Evaluate Lung Inflammation in Translational Research.Veterinary pathology · 2018Review
- The Potential Role of Trained Immunity in Autoimmune and Autoinflammatory Disorders.Frontiers in immunology · 2018Review
- In-silico modeling of granulomatous diseases.Current opinion in pulmonary medicine · 2016Review
- Epigenetics and Vasculitis: a Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- Epigenetics and Primary Biliary Cirrhosis: a Comprehensive Review and Implications for Autoimmunity.Clinical reviews in allergy & immunology · 2016Review
- Xenobiotics and loss of tolerance in primary biliary cholangitis.World journal of gastroenterology · 2016Review
- Extrahepatic malignancies in primary biliary cirrhosis: a comparative study at two European centers.Clinical reviews in allergy & immunology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune-mediated pulmonary diseases are a group of diseases that resulted from immune imbalance initiated by allergens or of unknown causes. Inflammatory responses without restrictions cause tissue damage and remodeling, which leads to airway hyperactivity, destruction of alveolar architecture, and a resultant loss of lung function. Epigenetic mechanisms have been demonstrated to be involved in inflammation, autoimmunity, and cancer. Recent studies have identified that epigenetic changes also regulate molecular pathways in immune-mediated lung diseases. Aberrant DNA methylation status, dysregulation of histone modifications, as well as altered microRNAs expression could change transcription activity of genes involved in the development of immune-mediated pulmonary diseases, which contributes to skewed differentiation of T cells and proliferation and activation of myofibroblasts, leading to overproduction of inflammatory cytokines and excessive accumulation of extracellular matrix, respectively. Aside from this, epigenetics also explains how environmental exposure influence on gene transcription without genetic changes. It acts as a mediator of the interaction between environmental factors and genetic factors. Identification of the abnormal epigenetic marks in diseases provides novel biomarkers for prediction and diagnosis and affords novel therapeutic targets for those difficult clinical problems, such as steroid-resistance and rapidly progressing fibrosis. In this review, we summarized the latest experimental and translational epigenetic studies in immune-mediated pulmonary diseases, including asthma, idiopathic pulmonary fibrosis, tuberculosis, sarcoidosis, and silicosis.
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.