ArticlePloS one2017
Activation of endoplasmic reticulum stress response by enhanced polyamine catabolism is important in the mediation of cisplatin-induced acute kidney injury.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Proteomic Profiling of Optic Nerves From SMOX-Deficient Mice Identifies Regulators of Neuroinflammation and Axonal Damage in Optic Neuritis.Investigative ophthalmology & visual science · 2026Article
- Multiplatform Metabolomic Profiling of the Unilateral Ureteral Obstruction Murine Model of CKD.International journal of molecular sciences · 2025Article
- Acute kidney injury through a metabolic lens: pathological reprogramming mechanisms and clinical translation potential.Frontiers in physiology · 2025Review
- Research progress and advances in endoplasmic reticulum stress regulation of acute kidney injury.Renal failure · 2024Review
- Polyamine Catabolism and Its Role in Renal Injury and Fibrosis in Mice Subjected to Repeated Low-Dose Cisplatin Treatment.Biomedicines · 2024Article
- Metabolism of Polyamines and Kidney Disease: A Promising Therapeutic Target.Kidney diseases (Basel, Switzerland) · 2023Review
- Spermidine from arginine metabolism activates Nrf2 and inhibits kidney fibrosis.Communications biology · 2023Article
- Transcriptome Analysis of Redox Systems and Polyamine Metabolic Pathway in Hepatoma and Non-Tumor Hepatocyte-like Cells.Biomolecules · 2023Article
- Exploring the Metabolic Differences between Cisplatin- and UV Light-Induced Apoptotic Bodies in HK-2 Cells by an Untargeted Metabolomics Approach.International journal of molecular sciences · 2023Article
- WR1065 conjugated to thiol-PEG polymers as novel anticancer prodrugs: broad spectrum efficacy, synergism, and drug resistance reversal.Frontiers in oncology · 2023Article
- Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury.Frontiers in cell and developmental biology · 2023Review
- Impact of renal tubularFrontiers in molecular biosciences · 2023Article
- Spermidine protects against acute kidney injury by modulating macrophage NLRP3 inflammasome activation and mitochondrial respiration in an eIF5A hypusination-related pathway.Molecular medicine (Cambridge, Mass.) · 2022Article
- Polyamines and Their Metabolism: From the Maintenance of Physiological Homeostasis to the Mediation of Disease.Medical sciences (Basel, Switzerland) · 2022Review
- Protective Role of Spermidine in Colitis and Colon Carcinogenesis.Gastroenterology · 2022Article
- Receptor of Advanced Glycation End Products Deficiency Attenuates Cisplatin-Induced Acute Nephrotoxicity by Inhibiting Apoptosis, Inflammation and Restoring Fatty Acid Oxidation.Frontiers in pharmacology · 2022Article
- Article
- Ablation of polyamine catabolic enzymes provokes Purkinje cell damage, neuroinflammation, and severe ataxia.Journal of neuroinflammation · 2020Article
- Polyamine Catabolism in Acute Kidney Injury.International journal of molecular sciences · 2019Review
- Deep insights into the response of human cervical carcinoma cells to a new cyano enone-bearing triterpenoid soloxolone methyl: a transcriptome analysis.Oncotarget · 2019Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Cisplatin-induced nephrotoxicity limits its use in many cancer patients. The expression of enzymes involved in polyamine catabolism, spermidine/spermine N1-acetyltransferase (SSAT) and spermine oxidase (SMOX) increase in the kidneys of mice treated with cisplatin. We hypothesized that enhanced polyamine catabolism contributes to tissue damage in cisplatin acute kidney injury (AKI). Using gene knockout and chemical inhibitors, the role of polyamine catabolism in cisplatin AKI was examined. Deficiency of SSAT, SMOX or neutralization of the toxic products of polyamine degradation, H2O2 and aminopropanal, significantly diminished the severity of cisplatin AKI. In vitro studies demonstrated that the induction of SSAT and elevated polyamine catabolism in cells increases the phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) and enhances the expression of binding immunoglobulin protein BiP/GRP78) and CCAAT-enhancer-binding protein homologous protein (CHOP/GADD153). The increased expression of these endoplasmic reticulum stress response (ERSR) markers was accompanied by the activation of caspase-3. These results suggest that enhanced polyamine degradation in cisplatin AKI may lead to tubular damage through the induction of ERSR and the consequent onset of apoptosis. In support of the above, we show that the ablation of the SSAT or SMOX gene, as well as the neutralization of polyamine catabolism products modulate the onset of ERSR (e.g. lower BiP and CHOP) and apoptosis (e.g. reduced activated caspase-3). These studies indicate that enhanced polyamine catabolism and its toxic products are important mediators of ERSR and critical to the pathogenesis of cisplatin AKI.
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