ReviewJournal of molecular medicine (Berlin, Germany)2022
Histone deacetylase 3 (HDAC3) as an important epigenetic regulator of kidney diseases.
Review in Journal of molecular medicine (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
The trial behind it
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Inhibition of histone deacetylase 3 alleviates lithocholic acid-induced intrahepatic cholestasis by enhancing expression of bile acid and lipid homeostasis-related genes.Acta pharmacologica Sinica · 2026Article
- Histone deacetylase 3‑mediated histone deacetylation combined with activating transcription factor 3 promotes renal fibrosis by inhibiting Klotho.Molecular medicine reports · 2026Article
- HDAC3-driven immunometabolic reprogramming in type 2 diabetes and its complications: from enzymatic deacetylation to non-enzymatic scaffolding.Frontiers in immunology · 2026Review
- Molecular frontiers in hemodialysis: unraveling the role of membranes in gene expression, epigenetics, and inflammatory pathways.International urology and nephrology · 2025Review
- Article
- Emerging epigenetic modifications in renal fibrosis: From mechanisms to treatments.Acta pharmaceutica Sinica. B · 2025Review
- HDAC3 knockdown inhibits ferroptosis via upregulating Nrf2 to alleviate renal interstitial fibrosis in lupus nephritis.Lupus science & medicine · 2025Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Review
- Epigenetic repurposing of carbohydrate metabolic inhibitors for insulin resistance: targeting DNMT1 and HDAC3 for β-cell restoration.Frontiers in epigenetics and epigenomics · 2025Review
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Advances in the Epigenetic Mechanisms of Diabetic Nephropathy Pathogenesis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Research Advances in Adenomyosis-Related Signaling Pathways and Promising Targets.Biomolecules · 2024Review
- Dually Modified Cellulose as a Non-Viral Vector for the Delivery and Uptake of HDAC3 siRNA.Pharmaceutics · 2023Article
- Application of Ligand- and Structure-Based Prediction Models for the Design of Alkylhydrazide-Based HDAC3 Inhibitors as Novel Anti-Cancer Compounds.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Review
- Functioning and mechanisms of PTMs in renal diseases.Frontiers in pharmacology · 2023Review
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- PDCD5 inhibits progression of renal cell carcinoma by promoting T cell immunity: with the involvement of the HDAC3/microRNA-195-5p/SGK1.Clinical epigenetics · 2022Article
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development and progression of many kidney diseases are substantially influenced by aberrant protein acetylation modifications of gene expression crucial for kidney functions. Histone deacetylase (HDAC) expression alterations are detected from renal samples of patients and animal models of various kidney diseases, and the administrations of HDAC inhibitors display impressive renal protective effects in vitro and in vivo. However, when the expression alterations of multiple HDACs occur, not all the HDACs causally affect the disease onset or progression. Identification of a single HDAC as a disease-causing factor will allow subtype-targeted intervention with less side effect. HDAC3 is a unique HDAC with distinct structural and subcellular distribution features and co-repressor dependency. HDAC3 is required for kidney development and its aberrations actively participate in many pathological processes, such as cancer, cardiovascular diseases, diabetes, and neurodegenerative disorders, and contribute significantly to the pathogenesis of kidney diseases. This review will discuss the recent studies that investigate the critical roles of HDAC3 aberrations in kidney development, renal aging, renal cell carcinoma, renal fibrosis, chronic kidney disease, polycystic kidney disease, glomerular podocyte injury, and diabetic nephropathy. These studies reveal the distinct characters of HDAC3 aberrations that act on different molecules/signaling pathways under various renal pathological conditions, which might shed lights into the epigenetic mechanisms of renal diseases and the potentially therapeutic strategies.
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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.