ArticleCells2022
HDAC6 Inhibition Alleviates Ischemia- and Cisplatin-Induced Acute Kidney Injury by Promoting Autophagy.
Article in Cells, 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, 31 citations in OpenAlex.
- Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026Review
- Regulation of organic anion transporting polypeptide 1B1 transport function by lysine deacetylase 6.Molecular pharmacology · 2026Article
- SIRT4 positively regulates autophagy via ULK1, but independently of HDAC6 and OPA1.FEBS open bio · 2026Article
- The tubulin code in acute ischemic stroke: post-translational reprogramming of the neuronal cytoskeleton and implications for phase-specific neuroprotection.Frontiers in neuroscience · 2026Review
- Electroacupuncture ameliorates diabetic renal injury by regulating the AMPK-autophagy signaling pathway.Iranian journal of basic medical sciences · 2026Article
- Yiqi-Wenyang-Tiaoshen Decoction Reduces Cisplatin-Induced Acute Kidney Injury in Rats Through Autophagy and Apoptosis Signaling Pathways Based on Network Pharmacology and Experimental Validation.Mediators of inflammation · 2026Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Network pharmacology combined with molecular docking and dynamics to assess the synergism of esculetin and phloretin against acute kidney injury-diabetes comorbidity.Molecular diversity · 2025Article
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Histone deacetylases: potential therapeutic targets in cisplatin-induced acute kidney injury.Annals of medicine · 2024Review
- Histone deacetylase expression following cisplatin-induced acute kidney injury in male and female mice.American journal of physiology. Renal physiology · 2024Article
- JianPiYiShen formula prevents cisplatin-induced acute kidney injury in mice by improving necroptosis through MAPK pathway.BMC complementary medicine and therapies · 2024Article
- Chronic hypoxia stabilizes 3βHSD1 via autophagy suppression.Cell reports · 2024Article
- Novel mechanistic study of HDAC6 regulation of rheumatoid arthritis via CMA: exploring potential therapeutic targets.Frontiers in pharmacology · 2024Article
- Flavin containing monooxygenase 2 regulates renal tubular cell fibrosis and paracrine secretion via SMURF2 in AKI‑CKD transformation.International journal of molecular medicine · 2023Article
- Emerging significance and therapeutic targets of ferroptosis: a potential avenue for human kidney diseases.Cell death & disease · 2023Review
- Inhibition of pyroptosis and apoptosis by capsaicin protects against LPS-induced acute kidney injury through TRPV1/UCP2 axisOpen life sciences · 2023Article
- HDAC6 inhibition: a significant potential regulator and therapeutic option to translate into clinical practice in renal transplantation.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase (HDAC) 6 exists exclusively in cytoplasm and deacetylates cytoplasmic proteins such as α-tubulin. HDAC6 dysfunction is associated with several pathological conditions in renal disorders, including UUO-induced fibrotic kidneys and rhabdomyolysis-induced nephropathy. However, the role of HDAC6 in ischemic acute kidney injury (AKI) and the mechanism by which HDAC6 inhibition protects tubular cells after AKI remain unclear. In the present study, we observed that HDAC6 was markedly activated in kidneys subjected to ischemia- and cisplatin (cis)-induced AKI treatment. Pharmacological inhibition of HDAC6 alleviated renal impairment and renal tubular damage after ischemia and cisplatin treatment. HDAC6 dysfunction was associated with decreased acetylation of α-tubulin at the residue of lysine 40 and autophagy. HDAC6 inhibition preserved acetyl-α-tubulin-enhanced autophagy flux in AKI and cultured tubular cells. Genetic ablation of the renal tubular (RT) Atg7 gene or pharmacological inhibition of autophagy suppressed the protective effects of HDAC6. Taken together, our study indicates that HDAC6 contributes to ischemia- and cisplatin-induced AKI by inhibiting autophagy and the acetylation of α-tubulin. These results suggest that HDAC6 could be a potential target for ischemic and nephrotoxic AKI.
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