ArticleNature communications2020
Histone deacetylase 3 controls lung alveolar macrophage development and homeostasis.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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, 43 citations in OpenAlex.
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Article
- Review
- The Role of HDAC3 in Pulmonary Diseases.Lung · 2025Review
- MicroRNAs regulate alveolar macrophage homeostasis and its function in lung fibrosis.Frontiers in immunology · 2025Article
- Identification and Characterization of Genes Associated with Intestinal Ischemia-Reperfusion Injury and Oxidative Stress: A Bioinformatics and Experimental Approach Integrating High-Throughput Sequencing, Machine Learning, and Validation.Journal of inflammation research · 2025Article
- HDAC3 in action: Expanding roles in inflammation and inflammatory diseases.Cell proliferation · 2025Review
- The role of alveolar macrophages in viral respiratory infections and their therapeutic implications.Biochemistry and biophysics reports · 2024Review
- Downregulation of IL-8 and IL-10 by LRRC8A Inhibition through the NOX2-Nrf2-CEBPB Transcriptional Axis in THP-1-Derived MInternational journal of molecular sciences · 2024Article
- Epigenetics and bronchopulmonary dysplasia: unraveling the complex interplay and potential therapeutic implications.Pediatric research · 2024Article
- HDAC1/2 and HDAC3 play distinct roles in controlling adult Meibomian gland homeostasis.The ocular surface · 2024Article
- Zinc-Dependent Histone Deacetylases in Lung Endothelial Pathobiology.Biomolecules · 2024Review
- The roles of tissue resident macrophages in health and cancer.Experimental hematology & oncology · 2024Review
- BRD3308 suppresses macrophage oxidative stress and pyroptosis via upregulating acetylation of H3K27 in sepsis-induced acute lung injury.Burns & trauma · 2024Article
- Single-Cell Profiling of Premature Neonate Airways Reveals a Continuum of Myeloid Differentiation.American journal of respiratory cell and molecular biology · 2023Article
- Article
- HDAC3 promotes macrophage pyroptosis via regulating histone deacetylation in acute lung injury.iScience · 2023Article
- The Role of Histone Deacetylases in Acute Lung Injury-Friend or Foe.International journal of molecular sciences · 2023Review
- The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases.Cell death discovery · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Alveolar macrophages (AMs) derived from embryonic precursors seed the lung before birth and self-maintain locally throughout adulthood, but are regenerated by bone marrow (BM) under stress conditions. However, the regulation of AM development and maintenance remains poorly understood. Here, we show that histone deacetylase 3 (HDAC3) is a key epigenetic factor required for AM embryonic development, postnatal homeostasis, maturation, and regeneration from BM. Loss of HDAC3 in early embryonic development affects AM development starting at E14.5, while loss of HDAC3 after birth affects AM homeostasis and maturation. Single-cell RNA sequencing analyses reveal four distinct AM sub-clusters and a dysregulated cluster-specific pathway in the HDAC3-deficient AMs. Moreover, HDAC3-deficient AMs exhibit severe mitochondrial oxidative dysfunction and deteriorative cell death. Mechanistically, HDAC3 directly binds to Pparg enhancers, and HDAC3 deficiency impairs Pparg expression and its signaling pathway. Our findings identify HDAC3 as a key epigenetic regulator of lung AM development and homeostasis.
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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.