ArticleInternational journal of molecular sciences2020
Trichostatin A Alleviates Renal Interstitial Fibrosis Through Modulation of the M2 Macrophage Subpopulation.
Article in International journal of molecular sciences, 2020. 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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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Antibody-lectin chimeras for glyco-immune checkpoint blockade.Nature biotechnology · 2026Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Decoding Macrophage Dynamics: A Pathway to Understanding and Treating Inflammatory Skin Diseases.International journal of molecular sciences · 2025Review
- Macrophage phenotypes modulate neoangiogenesis and fibroblast profiles in synovial-like organoid cultures.Osteoarthritis and cartilage · 2025Article
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Recent Advances of Trained immunity in Macrophages.International journal of biological sciences · 2025Review
- Histone Deacetylase (HDAC) Inhibitors as a Novel Therapeutic Option Against Fibrotic and Inflammatory Diseases.Biomolecules · 2024Review
- Lymphocytes and innate immune cells in acute kidney injury and repair.Nature reviews. Nephrology · 2024Review
- Role of miRNAs in macrophage-mediated kidney injury.Pediatric nephrology (Berlin, Germany) · 2024Review
- Targeting Macrophage Polarization for Reinstating Homeostasis following Tissue Damage.International journal of molecular sciences · 2024Review
- APC and ZBTB2 May Mediate M2 Macrophage Infiltration to Promote the Development of Renal Fibrosis: A Bioinformatics Analysis.BioMed research international · 2024Article
- Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023Review
- Potential therapeutic targets of macrophages in inhibiting immune damage and fibrotic processes in musculoskeletal diseases.Frontiers in immunology · 2023Review
- Gut Microbiota, Macrophages and Diet: An Intriguing New Triangle in Intestinal Fibrosis.Microorganisms · 2022Review
- Epithelial-mesenchymal transition in organ fibrosis development: current understanding and treatment strategies.Burns & trauma · 2022Review
- Molecular mechanisms of histone deacetylases and inhibitors in renal fibrosis progression.Frontiers in molecular biosciences · 2022Review
- Clec7a expression in inflammatory macrophages orchestrates progression of acute kidney injury.Frontiers in immunology · 2022Article
- Discovery of novel immunotherapeutic drug candidates for sciatic nerve injury using bioinformatic analysis and experimental verification.Frontiers in pharmacology · 2022Article
- Histone Acetylation and Modifiers in Renal Fibrosis.Frontiers in pharmacology · 2022Review
- Hypoxic mesenchymal stem cells ameliorate acute kidney ischemia-reperfusion injury via enhancing renal tubular autophagy.Stem cell research & therapy · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mounting evidence indicates that an increase in histone deacetylation contributes to renal fibrosis. Although inhibition of histone deacetylase (HDAC) can reduce the extent of fibrosis, whether HDAC inhibitors exert the antifibrotic effect through modulating the phenotypes of macrophages, the key regulator of renal fibrosis, remains unknown. Moreover, the functional roles of the M2 macrophage subpopulation in fibrotic kidney diseases remain incompletely understood. Herein, we investigated the role of HDAC inhibitors on renal fibrogenesis and macrophage plasticity. We found that HDAC inhibition by trichostatin A (TSA) reduced the accumulation of interstitial macrophages, suppressed the activation of myofibroblasts and attenuated the extent of fibrosis in obstructive nephropathy. Moreover, TSA inhibited M1 macrophages and augmented M2 macrophage infiltration in fibrotic kidney tissue. Interestingly, TSA preferentially upregulated M2c macrophages and suppressed M2a macrophages in the obstructed kidneys, which was correlated with a reduction of interstitial fibrosis. TSA also repressed the expression of proinflammatory and profibrotic molecules in cultured M2a macrophages and inhibited the activation of renal myofibroblasts. In conclusion, our study was the first to show that HDAC inhibition by TSA alleviates renal fibrosis in obstructed kidneys through facilitating an M1 to M2c macrophage transition.
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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.