ArticleAmerican journal of physiology. Lung cellular and molecular physiology2019
Histone deacetylase 6 regulates endothelial MyD88-dependent canonical TLR signaling, lung inflammation, and alveolar remodeling in the developing lung.
Article in American journal of physiology. Lung cellular and molecular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Global research progress of endothelial cells and ALI/ARDS: a bibliometric analysis.Frontiers in physiology · 2024Pooled it
- Ferroptosis-Pyroptosis Crosstalk in Spinal Cord Injury: Molecular Mechanisms, Emerging Connectors, and Staged Therapeutic Perspectives.Journal of molecular neuroscience : MN · 2026Review
- Prophylactic Inhaled Pattern Recognition Receptor Agonists Reprogram Lung Epithelial Response and Prevent Type 2 Allergic Inflammation.European journal of immunology · 2026Article
- The evolving pathophysiology of bronchopulmonary dysplasia.Physiological reviews · 2026Review
- The Role of Histone Modifications in Acute Lung Injury: Molecular Mechanisms and Potential of Traditional Chinese Medicine Treatment.Journal of inflammation research · 2026Review
- Defining endotypes of bronchopulmonary dysplasia in preterm infants to improve precision-based therapies.JCI insight · 2025Review
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Research progress of microvascular development in bronchopulmonary dysplasia.Pediatric investigation · 2024Review
- Epigenetic modifications in the development of bronchopulmonary dysplasia: a review.Pediatric research · 2024Review
- Zinc-Dependent Histone Deacetylases in Lung Endothelial Pathobiology.Biomolecules · 2024Review
- BAP31 Promotes Adhesion Between Endothelial Cells and Macrophages Through the NF-κB Signaling Pathway in Sepsis.Journal of inflammation research · 2024Article
- Advanced Progress of Histone Deacetylases in Rheumatic Diseases.Journal of inflammation research · 2024Review
- Post-translational modifications and bronchopulmonary dysplasia.Frontiers in pediatrics · 2024Review
- Article
- Insight into the lncRNA-mRNA Co-Expression Profile and ceRNA Network in Lipopolysaccharide-Induced Acute Lung Injury.Current issues in molecular biology · 2023Article
- The SARS-CoV-2 E protein induces Toll-like receptor 2-mediated neonatal lung injury in a model of COVID-19 viremia that is rescued by the glucocorticoid ciclesonide.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Angiopoietin-1 protects against endotoxin-induced neonatal lung injury and alveolar simplification in mice.Pediatric research · 2022Article
- Sp1 S-Sulfhydration Induced by Hydrogen Sulfide Inhibits Inflammation via HDAC6/MyD88/NF-κB Signaling Pathway in Adjuvant-Induced Arthritis.Antioxidants (Basel, Switzerland) · 2022Article
- Rhubarb Alleviates Acute Lung Injury by Modulating Gut Microbiota Dysbiosis in Mice.Current microbiology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Lung endothelial cell (EC) immune activation during bacterial sepsis contributes to acute lung injury and bronchopulmonary dysplasia in premature infants. The epigenetic regulators of sepsis-induced endothelial immune activation, lung inflammation, and alveolar remodeling remain unclear. Herein, we examined the role of the cytoplasmic histone deacetylase, HDAC6, in regulating EC Toll-like receptor 4 (TLR4) signaling and modulating sepsis-induced lung injury in a neonatal model of sterile sepsis. In human primary microvascular endothelial cells (HPMEC), lipopolysaccharide (LPS)-induced MAPK, IKK-β, and p65 phosphorylation as well as inflammatory cytokine expression were exaggerated with the HDAC6 inhibitor tubastatin A, and by dominant-negative HDAC6 with a mutated catalytic domain 2. Expression of HDAC6 wild-type protein suppressed LPS-induced myeloid differentiation primary response 88 (MyD88) acetylation, p65 (Lys
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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.