ArticleInternational journal of molecular medicine2018
Inhibition of histone deacetylase 1 ameliorates renal tubulointerstitial fibrosis via modulation of inflammation and extracellular matrix gene transcription in mice.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 42 citations in OpenAlex.
- Zinc Signaling in Acute Kidney Injury.Cells · 2026Review
- Fibroblast histone deacetylase-1 promotes kidney interstitial fibrosis following ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2026Article
- Function of epigenetic modifications in wound healing and potential therapies (Review).International journal of molecular medicine · 2025Review
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases.BMB reports · 2025Review
- Direct fibroblast reprogramming: an emerging strategy for treating organic fibrosis.Journal of translational medicine · 2025Review
- Epigenetic Regulation of Ferroptosis in Chronic Kidney Disease: Mechanisms and Implications.Research (Washington, D.C.) · 2025Review
- Epigenetic therapeutics attenuate kidney injury and fibrosis by restoring the expression of epigenetically reprogrammed fibrogenic genes and signaling pathways.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2025Article
- Epigenetic mechanisms differentially regulate blood pressure and renal dysfunction in male and female Npr1 haplotype mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Osteochondral Regeneration Ability of Uncultured Bone Marrow Mononuclear Cells and Platelet-Rich Fibrin Scaffold.Bioengineering (Basel, Switzerland) · 2023Article
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
- IL-27 induces autophagy through regulation of the DNMT1/lncRNA MEG3/ERK/p38 axis to reduce pulmonary fibrosis.Respiratory research · 2023Article
- Chronic scrotal heat stress causes testicular interstitial inflammation and fibrosis: An experimental study in mice.International journal of reproductive biomedicine · 2022Article
- Article
- 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
- Inhibition of Yes-Associated Protein by Verteporfin Ameliorates Unilateral Ureteral Obstruction-Induced Renal Tubulointerstitial Inflammation and Fibrosis.International journal of molecular sciences · 2020Article
- Application of Histone Deacetylase Inhibitors in Renal Interstitial Fibrosis.Kidney diseases (Basel, Switzerland) · 2020Review
- Extracellular S100A4 as a key player in fibrotic diseases.Journal of cellular and molecular medicine · 2020Review
- Histone Deacetylases in Kidney Physiology and Acute Kidney Injury.Seminars in nephrology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tubulointerstitial fibrosis is characterized by sustained inflammation and excessive extracellular matrix (ECM) accumulation, leading to chronic kidney disease. Valproic acid (VPA) has anticancer activity through regulation of cell differentiation and apoptosis via inhibition of histone deacetylase (HDAC) activity and is considered a class I HDAC inhibitor. In this study, the effect of VPA on unilateral ureteral obstruction (UUO)‑induced renal fibrosis by modulation of renal inflammation and ECM gene transcription was investigated. VPA treatment increased histone H3 acetylation in both sham‑ and UUO‑operated kidneys and decreased the UUO‑induced increase in tubular injury and ECM deposition in mice. VPA also decreased myofibroblast activation and proliferation in UUO kidneys and NRK‑49F cells. Finally, it was demonstrated that the anti‑fibrotic effect of VPA was associated with regulation of ECM protein promoter enrichment at an acetylated histone H3 site. In conclusion, the findings indicate that VPA may have a beneficial effect on UUO‑induced renal fibrosis via regulation of myofibroblast activation, proliferation, and ECM protein production by chromatin remodeling and ECM protein promoter transcription.
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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.