ArticleFrontiers in immunology2022
Pharmacologic Inhibition of Histone Deacetylase 6 Prevents the Progression of Chlorhexidine Gluconate-Induced Peritoneal Fibrosis by Blockade of M2 Macrophage Polarization.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Epigenetic programming of macrophages across inflammatory and malignant diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Research progress on histone deacetylases in peritoneal dialysis-associated peritoneal fibrosis.Renal failure · 2025Review
- Postbiotics Derived fromNutrients · 2025Article
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Peritoneal Dialysis -Associated Fibrosis: Emerging Mechanisms and Therapeutic Opportunities.Frontiers in pharmacology · 2025Review
- LCZ696, an angiotensin receptor-neprilysin inhibitor, ameliorates epithelial-mesenchymal transition of peritoneal mesothelial cells and M2 macrophage polarization.Renal failure · 2024Article
- The HDAC6 inhibitor AVS100 (SS208) induces a pro-inflammatory tumor microenvironment and potentiates immunotherapy.Science advances · 2024Article
- HDAC6-selective inhibitor CAY10603 ameliorates cigarette smoke-induced small airway remodeling by regulating epithelial barrier dysfunction and reversing.Respiratory research · 2024Article
- A narrative review of the role of HDAC6 in idiopathic pulmonary fibrosis.Journal of thoracic disease · 2024Review
- The disruptor of telomeric silencing 1-like (DOT1L) promotes peritoneal fibrosis through the upregulation and activation of protein tyrosine kinases.Molecular biomedicine · 2024Article
- Mechanisms underlying the involvement of peritoneal macrophages in the pathogenesis and novel therapeutic strategies for dialysis-induced peritoneal fibrosis.Frontiers in immunology · 2024Review
- Peritoneal fibrosis: from pathophysiological mechanism to medicine.Frontiers in physiology · 2024Review
- Unlocking Macrophage Secrets: Histone Deacetylases in Chronic Transplant Rejection.Results and problems in cell differentiation · 2024Review
- CGRP promotes osteogenic differentiation by regulating macrophage M2 polarization through HDAC6/AKAP12 signaling pathway.Regenerative medicine · 2024Article
- Unveiling the contribution of tumor-associated macrophages in driving epithelial-mesenchymal transition: a review of mechanisms and therapeutic Strategies.Frontiers in pharmacology · 2024Review
- Astragalus membranaceus and its monomers treat peritoneal fibrosis and related muscle atrophy through the AR/TGF-β1 pathway.Frontiers in pharmacology · 2024Article
- BET Protein Inhibitor JQ1 Ameliorates Experimental Peritoneal Damage by Inhibition of Inflammation and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- Brahma-related gene 1 acts as a profibrotic mediator and targeting it by micheliolide ameliorates peritoneal fibrosis.Journal of translational medicine · 2023Article
- Novel Aspects of the Immune Response Involved in the Peritoneal Damage in Chronic Kidney Disease Patients under Dialysis.International journal of molecular sciences · 2023Review
- Histone deacetylase 8 inhibition prevents the progression of peritoneal fibrosis by counteracting the epithelial-mesenchymal transition and blockade of M2 macrophage polarization.Frontiers in immunology · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peritoneal fibrosis contributes to ultrafiltration failure in peritoneal dialysis (PD) patients and thus restricts the wide application of PD in clinic. Recently we have demonstrated that histone deacetylase 6 (HDAC6) is critically implicated in high glucose peritoneal dialysis fluid (HG-PDF) induced peritoneal fibrosis, however, the precise mechanisms of HDAC6 in peritoneal fibrosis have not been elucidated. Here, we focused on the role and mechanisms of HDAC6 in chlorhexidine gluconate (CG) induced peritoneal fibrosis and discussed the mechanisms involved. We found Tubastatin A (TA), a selective inhibitor of HDAC6, significantly prevented the progression of peritoneal fibrosis, as characterized by reduction of epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) protein deposition. Inhibition of HDAC6 remarkably suppressed the expression of matrix metalloproteinases-2 (MMP2) and MMP-9. Administration of TA also increased the expression of acetylation Histone H3 and acetylation α-tubulin. Moreover, our results revealed that blockade of HDAC6 inhibited alternatively M2 macrophages polarization by suppressing the activation of TGF-β/Smad3, PI3K/AKT, and STAT3, STAT6 pathways. To give a better understanding of the mechanisms, we further established two cell injured models in Raw264.7 cells by using IL-4 and HG-PDF. Our
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