ArticleAmerican journal of physiology. Renal physiology2014
Class I HDAC activity is required for renal protection and regeneration after acute kidney injury.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Lactate and Lactylation in AKI-to-CKD: Epigenetic Regulation and Therapeutic Opportunities.Cell proliferation · 2025Review
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- The role of resistin and adiponectin ratios with uric acid in assessing metabolic syndrome in type 2 diabetes.Molecular and cellular biochemistry · 2025Article
- Lactate metabolism and acute kidney injury.Chinese medical journal · 2025Review
- Acquired vulnerability against EGF receptor inhibition in gastric cancer promoted by class I histone deacetylase inhibitor entinostat.Neoplasia (New York, N.Y.) · 2025Article
- Protein lactylation in kidney diseases.Frontiers in cell and developmental biology · 2025Review
- Histone deacetylase expression following cisplatin-induced acute kidney injury in male and female mice.American journal of physiology. Renal physiology · 2024Article
- Targeting the epidermal growth factor receptor (EGFR/ErbB) for the potential treatment of renal pathologies.Frontiers in pharmacology · 2024Review
- Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023Review
- Pharmacological inhibition of the mixed lineage leukemia 1-menin interaction aggravates acute kidney injury induced by folic acid and ischemia-reperfusion in mice.American journal of physiology. Renal physiology · 2023Article
- VPA improves ferroptosis in tubular epithelial cells after cisplatin-induced acute kidney injury.Frontiers in pharmacology · 2023Article
- Histone Modifications in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2022Review
- Epigenetic regulation of Toll-like receptors 2 and 4 in kidney disease.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Validation of HDAC8 Inhibitors as Drug Discovery Starting Points to Treat Acute Kidney Injury.ACS pharmacology & translational science · 2022Article
- Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition.Pharmaceuticals (Basel, Switzerland) · 2022Review
- The Role and Mechanism of Histone Deacetylases in Acute Kidney Injury.Frontiers in pharmacology · 2021Review
- Class IIa HDAC inhibitor TMP195 alleviates lipopolysaccharide-induced acute kidney injury.American journal of physiology. Renal physiology · 2020Article
- HDAC1-mediated deacetylation of LSD1 regulates vascular calcification by promoting autophagy in chronic renal failure.Journal of cellular and molecular medicine · 2020Article
- Histone Deacetylases in Kidney Physiology and Acute Kidney Injury.Seminars in nephrology · 2020Review
- Dynamic changes in histone deacetylases following kidney ischemia-reperfusion injury are critical for promoting proximal tubule proliferation.American journal of physiology. Renal physiology · 2019Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Activation of histone deacetylases (HDACs) is required for renal epithelial cell proliferation and kidney development. However, their role in renal tubular cell survival and regeneration after acute kidney injury (AKI) remains unclear. In this study, we demonstrated that all class I HDAC isoforms (1, 2, 3, and 8) were expressed in the renal epithelial cells of the mouse kidney. Inhibition of class I HDACs with MS-275, a highly selective inhibitor, resulted in more severe tubular injury in the mouse model of AKI induced by folic acid or rhabdomyolysis, as indicated by worsening renal dysfunction, increased neutrophil gelatinase-associated lipocalin expression, and enhanced apoptosis and caspase-3 activation. Blocking class I HDAC activity also impaired renal regeneration as evidenced by decreased expression of renal Pax-2, vimentin, and proliferating cell nuclear antigen. Injury to the kidney is accompanied by increased phosphorylation of epidermal growth factor receptor (EGFR), signal transducers and activators of transcription 3 (STAT3), and Akt. Inhibition of class I HDACs suppressed EGFR phosphorylation as well as reduced its expression. MS-275 was also effective in inhibiting STAT3 and Akt phosphorylation, but this treatment did not affect their expression levels. Taken together, these data suggest that the class I HDAC activity contributes to renal protection and functional recovery and is required for renal regeneration after AKI. Furthermore, renal EGFR signaling is subject to regulation by this class of HDACs.
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