ArticleFrontiers in immunology2020
HDAC6 Mediates Macrophage iNOS Expression and Excessive Nitric Oxide Production in the Blood During Endotoxemia.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- HDAC6 Promotes Host Defense Against Chlamydial Lung Infections by Regulating M2-Th2 Responses.International journal of molecular sciences · 2026Article
- HDAC6 inhibition reprograms endothelial and macrophage responses to protect the lung in endotoxemia.Respiratory research · 2026Article
- Taurine Intake Alleviates Oxidative Damage During Transportation inAnimals : an open access journal from MDPI · 2026Article
- Article
- HDAC6 Deletion Decreases Pristane-induced Inflammation.ImmunoHorizons · 2024Article
- Lack of effect from genetic deletion of Hdac6 in a humanized mouse model of CMT2D.Journal of the peripheral nervous system : JPNS · 2024Article
- ANKRD22 aggravates sepsis-induced ARDS and promotes pulmonary M1 macrophage polarization.Journal of translational autoimmunity · 2024Article
- HDAC6 inhibitor ACY-1215 enhances STAT1 acetylation to block PD-L1 for colorectal cancer immunotherapy.Cancer immunology, immunotherapy : CII · 2024Article
- Amentoflavone for treating cardiocerebrovascular diseases and neurological disorders.Frontiers in pharmacology · 2024Review
- The Role of Histone Deacetylases in Acute Lung Injury-Friend or Foe.International journal of molecular sciences · 2023Review
- Neuronal nitric oxide synthase is required for erythropoietin stimulated erythropoiesis in mice.Frontiers in cell and developmental biology · 2023Article
- Article
- Molecular Targets of Brown Algae Phlorotannins for the Therapy of Inflammatory Processes of Various Origins.Marine drugs · 2022Review
- Review
- Effect of NOS Inhibitors and Anticoagulants on Nitric Oxide Production in a Tissue-factor Induced Rat DIC Model.In vivo (Athens, Greece)Article
- Innate Immune Memory in Macrophages.Newborn (Clarksville, Md.)Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Excessive nitric oxide (NO) production and NO-mediated nitrative stress contribute to vascular dysfunction, inflammation, and tissue injury in septic shock. New therapeutic targets are urgently needed to provide better control of NO level during septic shock. In the present study, we investigated the role of HDAC6 in the regulation of NO production and nitrative stress in a mouse model of endotoxin-induced septic shock. HDAC6 deficient mice and a specific HDAC6 inhibitor were utilized in our studies. Our data clearly indicate that HDAC6 is an important mediator of NO production in macrophages. HDAC6 mediates NO production through the regulation of iNOS expression in macrophages. HDAC6 up-regulates iNOS expression in macrophages by modulating STAT1 activation and IRF-1 expression. HDAC6 inhibition potently blocked endotoxin-induced STAT1 activation and iNOS expression in macrophages. Furthermore, HDAC6 contributes to excessive NO production and nitrotyrosine level in the blood and promotes iNOS expression in the lung tissues during septic shock. Our data reveal a novel HDAC6/STAT1/iNOS pathway that mediates excessive NO production and nitrative stress in septic shock.
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Registered trials
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