ReviewFrontiers in molecular biosciences2022
Molecular mechanisms of histone deacetylases and inhibitors in renal fibrosis progression.
Review in Frontiers in molecular biosciences, 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, 38 citations in OpenAlex.
- A Circuit of Mechanically Regulated Transcription Factors Balances Regenerative and Fibrotic Memory of Mesenchymal Stromal Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Role and Therapeutic Potential of the STING Signaling Pathway in the Pathogenesis of Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Review
- Indoxyl sulfate in the gut-kidney axis: from diet-microbiome interactions to renal injury and targeted therapies.Frontiers in nutrition · 2026Review
- Epigenetic Suppression of RASAL1 by HDAC3 and Cofactor YY1 Promotes Fibroblast-Myofibroblast Transition and Renal Fibrosis.Research (Washington, D.C.) · 2026Article
- 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
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Gut microbiota-derived short-chain fatty acids mediate the antifibrotic effects of traditional Chinese medicine in diabetic nephropathy.Frontiers in endocrinology · 2025Review
- Histone Deacetylase (HDAC) Inhibitors as a Novel Therapeutic Option Against Fibrotic and Inflammatory Diseases.Biomolecules · 2024Review
- Epigenetic Regulation in Myocardial Fibroblasts and Its Impact on Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- METTL3-Mediated N 6 -Methyladenosine mRNA Modification and cGAS-STING Pathway Activity in Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2024Article
- Epigenetic and Metabolic Reprogramming of Fibroblasts in Crohn's Disease Strictures Reveals Histone Deacetylases as Therapeutic Targets.Journal of Crohn's & colitis · 2024Article
- Targeting the epidermal growth factor receptor (EGFR/ErbB) for the potential treatment of renal pathologies.Frontiers in pharmacology · 2024Review
- Advances in the study of key cells and signaling pathways in renal fibrosis and the interventional role of Chinese medicines.Frontiers in pharmacology · 2024Review
- Cell and rat serum, urine and tissue metabolomics analysis elucidates the key pathway changes associated with chronic nephropathy and reveals the mechanism of action of rhein.Chinese medicine · 2023Article
- Minichromosome maintenance 6 protects against renal fibrogenesis by regulating DUSP6-mediated ERK/GSK-3β/Snail1 signaling.iScience · 2023Article
- HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice.Nature communications · 2023Article
- HDAC11, an emerging therapeutic target for metabolic disorders.Frontiers in endocrinology · 2022Review
- Renal Mast Cell-Specific Proteases in the Pathogenesis of Tubulointerstitial Fibrosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry SocietyArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis is a common progressive manifestation of chronic kidney disease. This phenomenon of self-repair in response to kidney damage seriously affects the normal filtration function of the kidney. Yet, there are no specific treatments for the condition, which marks fibrosis as an irreversible pathological sequela. As such, there is a pressing need to improve our understanding of how fibrosis develops at the cellular and molecular levels and explore specific targeted therapies for these pathogenic mechanisms. It is now generally accepted that renal fibrosis is a pathological transition mediated by extracellular matrix (ECM) deposition, abnormal activation of myofibroblasts, and epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells under the regulation of TGF-β. Histone deacetylases (HDACs) appear to play an essential role in promoting renal fibrosis through non-histone epigenetic modifications. In this review, we summarize the mechanisms of renal fibrosis and the signaling pathways that might be involved in HDACs in renal fibrosis, and the specific mechanisms of action of various HDAC inhibitors (HDACi) in the anti-fibrotic process to elucidate HDACi as a novel therapeutic tool to slow down the progression of renal fibrosis.
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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.