ArticleAmerican journal of physiology. Renal physiology2020
Class IIa HDAC inhibitor TMP195 alleviates lipopolysaccharide-induced acute kidney injury.
Article in American journal of physiology. Renal physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- New trends and hotspots in sepsis-related protein post-translational modification: a bibliometric and visual analysis.Frontiers in medicine · 2025Pooled it
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Epigenetics-mediated pathological alterations and their diagnostic and therapeutic potential in sepsis-associated acute kidney injury.Clinical epigenetics · 2026Review
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Lactylation in kidney diseases: a review of regulatory mechanisms and therapeutic prospects.Frontiers in cell and developmental biology · 2026Review
- HDAC5 Inhibition as a Therapeutic Strategy for Titin Deficiency-Induced Cardiac Remodeling: Insights from Human iPSC Models.Medicines (Basel, Switzerland) · 2025Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- HDAC4: an emerging target in diabetes mellitus and diabetic complications.European journal of medical research · 2025Review
- Discovery of a potential hematologic malignancies therapy: Selective and potent HDAC7 PROTAC degrader targeting non-enzymatic function.Acta pharmaceutica Sinica. B · 2025Article
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Review of research progress in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2025Review
- EP300-mediated H3 acetylation elevates MTHFD2 expression to reduce mitochondrial dysfunction in lipopolysaccharide-induced tubular epithelial cells.Renal failure · 2024Article
- Human Umbilical Cord-Derived Mesenchymal Stem Cells-Exosomes-Delivered miR-375 Targets HDAC4 to Promote Autophagy and Suppress T Cell Apoptosis in Sepsis-Associated Acute Kidney Injury.Applied biochemistry and biotechnology · 2024Article
- mPPTMP195 nanoparticles enhance fracture recovery through HDAC4 nuclear translocation inhibition.Journal of nanobiotechnology · 2024Article
- Post-translational modifications in sepsis-induced organ dysfunction: mechanisms and implications.Frontiers in immunology · 2024Review
- Effect of HDAC9 on the differentiation of chicken embryonic stem cells into male germ cells.Animal reproduction · 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
- Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Sepsis-associated acute kidney injury (SA-AKI) is associated with high mortality rates, but clinicians lack effective treatments except supportive care or renal replacement therapies. Recently, histone deacetylase (HDAC) inhibitors have been recognized as potential treatments for acute kidney injury and sepsis in animal models; however, the adverse effect generated by the use of pan inhibitors of HDACs may limit their application in people. In the present study, we explored the possible renoprotective effect of a selective class IIa HDAC inhibitor, TMP195, in a murine model of SA-AKI induced by lipopolysaccharide (LPS). Administration of TMP195 significantly reduced increased serum creatinine and blood urea nitrogen levels and renal damage induced by LPS; this was coincident with reduced expression of HDAC4, a major isoform of class IIa HDACs, and elevated histone H3 acetylation. TMP195 treatment following LPS exposure also reduced renal tubular cell apoptosis and attenuated renal expression of neutrophil gelatinase-associated lipocalin and kidney injury molecule-1, two biomarkers of tubular injury. Moreover, LPS exposure resulted in increased expression of BAX and cleaved caspase-3 and decreased expression of Bcl-2 and bone morphogenetic protein-7 in vivo and in vitro; TMP195 treatment reversed these responses. Finally, TMP195 inhibited LPS-induced upregulation of multiple proinflammatory cytokines/chemokines, including intercellular adhesion molecule-1, monocyte chemoattractant protein-1, tumor necrosis factor-α, and interleukin-1β, and accumulation of inflammatory cells in the injured kidney. Collectively, these data indicate that TMP195 has a powerful renoprotective effect in SA-AKI by mitigating renal tubular cell apoptosis and inflammation and suggest that targeting class IIa HDACs might be a novel therapeutic strategy for the treatment of SA-AKI that avoids the unintended adverse effects of a pan-HDAC inhibitor.
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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.