ArticleNature immunology2015
The microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote T(H)17 cell-dependent emphysema.
Article in Nature immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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.
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Who cites it
68 citing papers in PubMed, 114 citations in OpenAlex.
- Hallmarks of lung cancer driven by inhalable particulate matter: From cell-intrinsic oncogenic traits to microenvironment remodeling.Innovation (Cambridge (Mass.)) · 2026Review
- The role and mechanism of histone deacetylase in COPD.Molecular and cellular biochemistry · 2026Review
- The role of viral infection in implantation failure: direct and indirect effects.Reproductive biology and endocrinology : RB&E · 2024Review
- Downregulation ofeLife · 2024Article
- Class IIa HDAC4 and HDAC7 cooperatively regulate gene transcription in Th17 cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Downregulation ofbioRxiv : the preprint server for biology · 2024Article
- MicroRNAs as Potential Biomarkers of Environmental Exposure to Polycyclic Aromatic Hydrocarbons and Their Link with Inflammation and Lung Cancer.International journal of molecular sciences · 2023Review
- Is there a potential of circulating miRNAs as biomarkers in rheumatic diseases?Genes & diseases · 2023Review
- Air Pollution and microRNAs: The Role of Association in Airway Inflammation.Life (Basel, Switzerland) · 2023Review
- miR-22 gene therapy treats HCC by promoting anti-tumor immunity and enhancing metabolism.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Profiling of Circulating Tumor Cells for Screening of Selective Inhibitors of Tumor-Initiating Stem-Like Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Insights into the toxicological effects of nanomaterials on atherosclerosis: mechanisms involved and influence factors.Journal of nanobiotechnology · 2023Review
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Nutriepigenomics in Environmental-Associated Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- Impact of extracellular vesicles on the pathogenesis, diagnosis, and potential therapy in cardiopulmonary disease.Frontiers in pharmacology · 2023Review
- Review
- Milk-Derived miR-22-3p Promotes Proliferation of Human Intestinal Epithelial Cells (HIECs) by Regulating Gene Expression.Nutrients · 2022Article
- Chronic exposure to carbon black ultrafine particles reprograms macrophage metabolism and accelerates lung cancer.Science advances · 2022Article
- Article
- Stress-Induced Immunosuppression Affects Immune Response to Newcastle Disease Virus Vaccine via Circulating miRNAs.Animals : an open access journal from MDPI · 2022Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Smoking-related emphysema is a chronic inflammatory disease driven by the T(H)17 subset of helper T cells through molecular mechanisms that remain obscure. Here we explored the role of the microRNA miR-22 in emphysema. We found that miR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism that involved the transcription factor NF-κB. Mice deficient in miR-22, but not wild-type mice, showed attenuated T(H)17 responses and failed to develop emphysema after exposure to smoke or nCB. We further found that miR-22 controlled the activation of APCs and T(H)17 responses through the activation of AP-1 transcription factor complexes and the histone deacetylase HDAC4. Thus, miR-22 is a critical regulator of both emphysema and T(H)17 responses.
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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.