ArticleJournal of the American Society of Nephrology : JASN2013
Histone deacetylase inhibitor enhances recovery after AKI.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
110 citing papers in PubMed, 185 citations in OpenAlex.
- SLC38A6 expression in renal tubular cells accelerates cisplatin-induced acute kidney injury by promoting cell apoptosis.The FEBS journal · 2026Article
- Fibroblast histone deacetylase-1 promotes kidney interstitial fibrosis following ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2026Article
- Article
- Erythropoiesis-Stimulating Agent Protects Against Kidney Fibrosis by Inhibiting G2/M Cell Cycle Arrest.Cells · 2025Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
- Lactate metabolism and acute kidney injury.Chinese medical journal · 2025Review
- Three- and four-stranded nucleic acid structures and their ligands.RSC chemical biology · 2025Review
- Assays to measure small molecule Hsp70 agonist activity in vitro and in vivo.Analytical biochemistry · 2025Article
- Enzymatic post-translational modifications of proteins in chronic kidney disease: mechanisms, regulation, and clinical significance.Frontiers in pharmacology · 2025Review
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Senescence and SASP Are Potential Therapeutic Targets for Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Exosomal miR-223-3p from bone marrow mesenchymal stem cells targets HDAC2 to downregulate STAT3 phosphorylation to alleviate HBx-induced ferroptosis in podocytes.Frontiers in pharmacology · 2024Article
- [Role of Histone Modifications in Acute Kidney Injury Progressing to Chronic Kidney Disease].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Article
- Subpopulations of hypocretin/orexin neurons differ in measures of their cell proliferation, dynorphin co-expression, projections, and response to embryonic ethanol exposure.Scientific reports · 2023Article
- SARS-CoV-2 viral protein ORF3A injures renal tubules by interacting with TRIM59 to induce STAT3 activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Review
- Bibliometric and visualization analysis of kidney repair associated with acute kidney injury from 2002 to 2022.Frontiers in pharmacology · 2023Article
- Histone Modifications in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2022Review
- Cellular senescence in ischemia/reperfusion injury.Cell death discovery · 2022Review
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
At present, there are no effective therapies to ameliorate injury, accelerate recovery, or prevent postinjury fibrosis after AKI. Here, we sought to identify candidate compounds that accelerate recovery after AKI by screening for small molecules that increase proliferation of renal progenitor cells in zebrafish embryos. One compound identified from this screen was the histone deacetylase inhibitor methyl-4-(phenylthio)butanoate, which we subsequently administered to zebrafish larvae and mice 24-48 hours after inducing AKI. In zebrafish, treatment with the compound increased larval survival and proliferation of renal tubular epithelial cells. In mice, treatment accelerated recovery, reduced postinjury tubular atrophy and interstitial fibrosis, and increased the regenerative capacity of actively cycling renal tubular cells by decreasing the number of cells in G2/M arrest. These data suggest that accelerating recovery may be a viable approach to treating AKI and provide proof of concept that a screen in zebrafish embryos can identify therapeutic candidates for kidney injury.
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What OpenQuestion holds
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.