ArticleRespiratory research2018
Inhibition of histone-deacetylase activity rescues inflammatory cystic fibrosis lung disease by modulating innate and adaptive immune responses.
Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 36 citations in OpenAlex.
- Epigenetic regulation and chromatin organization in cystic fibrosis airways.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Review
- Correction of a Traffic-Defective Missense ABCB11 Variant Responsible for Progressive Familial Intrahepatic Cholestasis Type 2.International journal of molecular sciences · 2025Article
- SAHA inhibits lung fibroblast activation by increasing p66Shc expression epigenetically.Aging medicine (Milton (N.S.W)) · 2024Article
- A New Frontier in Cystic Fibrosis Pathophysiology: How and When Clock Genes Can Affect the Inflammatory/Immune Response in a Genetic Disease Model.Current issues in molecular biology · 2024Review
- Deacetylation of Histones and Non-histone Proteins in Inflammatory Diseases and Cancer Therapeutic Potential of Histone Deacetylase Inhibitors.Current genomics · 2023Review
- In vivo impact of tubulin polymerization promoting protein (Tppp) knockout to the airway inflammatory response.Scientific reports · 2023Article
- The main protease of SARS-CoV-2 cleaves histone deacetylases and DCP1A, attenuating the immune defense of the interferon-stimulated genes.The Journal of biological chemistry · 2023Article
- Therapeutic Efficacy of Novel HDAC Inhibitors SPA3052 and SPA3074 against Intestinal Inflammation in a Murine Model of Colitis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Article
- Chasing a Breath of Fresh Air in Cystic Fibrosis (CF): Therapeutic Potential of Selective HDAC6 Inhibitors to Tackle Multiple Pathways in CF Pathophysiology.Journal of medicinal chemistry · 2022Review
- Multifocal Organoid Capturing of Colon Cancer Reveals Pervasive Intratumoral Heterogenous Drug Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Role of Histone Post-Translational Modifications in Inflammatory Diseases.Frontiers in immunology · 2022Review
- Prognosis-Based Early Intervention Strategies to Resolve Exacerbation and Progressive Lung Function Decline in Cystic Fibrosis.Journal of personalized medicine · 2021Article
- Preclinical and clinical progress for HDAC as a putative target for epigenetic remodeling and functionality of immune cells.International journal of biological sciences · 2021Review
- Histone Deacetylation Inhibitors as Modulators of Regulatory T Cells.International journal of molecular sciences · 2020Review
- Mining GWAS and eQTL data for CF lung disease modifiers by gene expression imputation.PloS one · 2020Article
- HDAC6 depletion improves cystic fibrosis mouse airway responses to bacterial challenge.Scientific reports · 2019Article
- HDAC inhibitors rescue multiple disease-causing CFTR variants.Human molecular genetics · 2019Article
- Trichostatin A‑induced miR‑30a‑5p regulates apoptosis and proliferation of keloid fibroblasts via targeting BCL2.Molecular medicine reports · 2019Article
- Transcriptional consequences of impaired immune cell responses induced by cystic fibrosis plasma characterized via dual RNA sequencing.BMC medical genomics · 2019Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundChronic lung disease resulting from dysfunctional cystic fibrosis transmembrane conductance regulator (CFTR) and NFκB-mediated neutrophilic-inflammation forms the basis of CF-related mortality. Here we aimed to evaluate if HDAC inhibition controls Pseudomonas-aeruginosa-lipopolysaccharide (Pa-LPS) induced airway inflammation and CF-lung disease.
methodsFor in vitro experiments, HEK293-cells were transfected with IL-8 or NFκB-firefly luciferase, and SV40-renilla- luciferase reporter constructs or ΔF508-CFTR-pCEP, followed by treatment with suberoylanilide hydroxamic acid (SAHA), Trichostatin-A (TSA) and/or TNFα. For murine studies, Cftr
resultsSAHA treatment significantly (p < 0.05) suppresses TNFα-induced NFκB and IL-8 reporter activities in HEK293-cells. Moreover, SAHA, Tubacin (selective HDAC6-inhibitor) or HDAC6-shRNAs controls CSE-induced ER-stress activities (p < 0.05). In addition, SAHA restores trafficking of misfolded-ΔF508-CFTR, by inducing protein levels of both B and C forms of CFTR. Murine studies using Cftr
conclusionIn summary, SAHA-mediated HDAC inhibition modulates innate and adaptive immune responses involved in pathogenesis and progression of inflammatory CF-lung disease.
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