ArticleScientific reports2016
Silencing of Histone Deacetylase 9 Expression in Podocytes Attenuates Kidney Injury in Diabetic Nephropathy.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 31 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.
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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
31 citing papers in PubMed, 47 citations in OpenAlex.
- PUM2 Lowers HDAC9 mRNA Stability to Improve Contrast-Induced Acute Kidney Injury by Attenuating Oxidative Stress and Promoting Autophagy.Diabetes & metabolism journal · 2026Article
- Article
- Retraction: Knockdown of TRIM65 inhibits lung cancer cell proliferation, migration and invasion: A therapeutic target in human lung cancer.Oncotarget · 2024Article
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Identification of HDAC9 and ARRDC4 as potential biomarkers and targets for treatment of type 2 diabetes.Scientific reports · 2024Article
- DNA methylation of miR-181a-5p mediated by DNMT3b drives renal interstitial fibrosis developed from acute kidney injury.Epigenomics · 2024Article
- [Inhibition of Histone Deacetylase 6 Ameliorates Podocyte Injury in Diabetic Kidney Disease in Mice].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Article
- Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023Review
- Knockdown of histone deacetylase 9 attenuates sepsis-induced myocardial injury and inflammatory response.Experimental animals · 2023Article
- HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice.Nature communications · 2023Article
- The Potential Biotherapeutic Targets of Contrast-Induced Acute Kidney Injury.International journal of molecular sciences · 2023Review
- ATF5 regulates tubulointerstitial injury in diabetic kidney disease via mitochondrial unfolded protein response.Molecular medicine (Cambridge, Mass.) · 2023Article
- Histone modification in podocyte injury of diabetic nephropathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- The Dynamics and Plasticity of Epigenetics in Diabetic Kidney Disease: Therapeutic Applications Vis-à-Vis.International journal of molecular sciences · 2022Review
- Knockdown of HDAC9 Inhibits Osteogenic Differentiation of Human Bone Marrow Mesenchymal Stem Cells Partially by Suppressing the MAPK Signaling Pathway.Clinical interventions in aging · 2022Article
- A New Prospect for the Treatment of Nephrotic Syndrome Based on Network Pharmacology Analysis.Current research in physiology · 2022Article
- Selective Inhibition of Histone Deacetylase Class IIa With MC1568 Ameliorates Podocyte Injury.Frontiers in medicine · 2022Article
- Inhibition of HDAC6 With CAY10603 Ameliorates Diabetic Kidney Disease by Suppressing NLRP3 Inflammasome.Frontiers in pharmacology · 2022Article
- Review
- Effects of metabolic memory on inflammation and fibrosis associated with diabetic kidney disease: an epigenetic perspective.Clinical epigenetics · 2021Review
Corrections and comments
- Retraction · 2024-04-02Concerns/Issues about Image · Duplication of/in Image · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions · · See also: https://pubpeer.com/publications/0DDF28DED193AFE08FF03586F75772
- Retracted
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocyte dysfunction is important in the onset and development of diabetic nephropathy (DN). Histone deacetylases (HDACs) have been recently proved to play critical roles in the pathogenesis of DN. As one subtype of the class IIa HDACs, HDAC9 is capable to repress/de-repress their target genes in tumor, inflammation, atherosclerosis and metabolic diseases. In the present study, we investigate whether HDAC9 is involved in the pathophysiologic process of DN, especially the podocyte injury. Firstly, we explored the expression patterns and localization of HDAC9 and found that HDAC9 expression was significantly up-regulated in high glucose (HG)-treated mouse podocytes, as well as kidney tissues from diabetic db/db mice and patients with DN. Secondly, knockdown of HDAC9 in mouse podocytes significantly suppressed HG-induced reactive oxygen species (ROS) generation, cell apoptosis and inflammation through JAK2/STAT3 pathway and reduced the podocytes injury by decreasing the expression levels of Nephrin and Podocin. Moreover, in diabetic db/db mice, silencing of HDAC9 attenuated the glomerulosclerosis, inflammatory cytokine release, podocyte apoptosis and renal injury. Collectively, these data indicate that HDAC9 may be involved in the process of DN, especially podocyte injury. Our study suggest that inhibition of HDAC9 may have a therapeutic potential in DN treatment.
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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.