ArticlePloS one2014
Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- The Role of Metabolites in Acyclovir-Induced Neurotoxicity and Nephrotoxicity.Medicines (Basel, Switzerland) · 2026Review
- Clinical Review of Risk of Nephrotoxicity with Acyclovir Use for Treatment of Herpes Simplex Virus Infections in Neonates and Children.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2023Article
- Central Composite Design for Formulation and Optimization of Solid Lipid Nanoparticles to Enhance Oral Bioavailability of Acyclovir.Molecules (Basel, Switzerland) · 2021Article
- Transdermal Film Loaded with Garlic Oil-Acyclovir Nanoemulsion to Overcome Barriers for Its Use in Alleviating Cold Sore Conditions.Pharmaceutics · 2021Article
- Acyclovir-Loaded Solid Lipid Nanoparticles: Optimization, Characterization and Evaluation of Its Pharmacokinetic Profile.Nanomaterials (Basel, Switzerland) · 2020Article
- The combination of acyclovir and dexamethasone protects against Alzheimer's disease-related cognitive impairments in mice.Psychopharmacology · 2020Article
- Leflunomide increased the renal exposure of acyclovir by inhibiting OAT1/3 and MRP2.Acta pharmacologica Sinica · 2020Article
- Identification of Novel Biomarkers for Predicting Kidney Injury Due to Drugs Using "Omic" Strategies.Pharmacogenomics and personalized medicine · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acyclovir (ACV) is an effective and widely used antiviral agent. However, its clinical application is limited by severe nephrotoxicity. We assessed ACV-induced nephrotoxicity and identified the differentially expressed proteins using mass spectrometry-based proteomic analysis. In total, 30 ICR mice were intraperitoneally administrated ACV (150 or 600 mg/kg per day) for 9 days. After administration of ACV, levels of serum creatinine and urea nitrogen increased significantly. In addition, mouse kidneys exhibited histopathological changes and reduced expression levels of vascular endothelial growth factor (VEGF) and its receptor VEGFR2. In the proteomic analysis, more than 1,000 proteins were separated by two-dimensional polyacrylamide gel electrophoresis, and a total of 20 proteins were up- or down-regulated in the ACV group compared with the saline group. Among these, six proteins (MHC class II antigen, glyoxalase 1, peroxiredoxin 1, αB-crystallin, fibroblast growth factor receptor 1-IIIb, and cytochrome c oxidase subunit Vb) were identified in association with ACV-induced nephrotoxicity. These findings were confirmed by Western blotting analysis. The differential expression levels of α-BC, Prx1, Glo I and CcO Vb suggest that oxidative damage and mitochondrial injury may be involved in ACV-induced nephrotoxicity. Furthermore, VEGF and FGF may play a role in tissue repair and the restoration process following ACV nephrotoxicity.
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Registered trials
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