ArticleAmerican journal of physiology. Cell physiology2010
The role of spermidine/spermine N1-acetyltransferase in endotoxin-induced acute kidney injury.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Sensitizing Colorectal Cancer to PARP Inhibitors: Biomarkers, Mechanisms, and Combination Strategies.International journal of molecular sciences · 2026Review
- Polyamine metabolism in ischemia reperfusion injury: common mitochondrial mechanisms and organ-specific differences.Journal of translational medicine · 2026Review
- Untangling amino acid metabolism in renal diseases: mechanisms, dysregulation, and critical gaps.Clinical kidney journal · 2026Review
- MicroRNA-382 Is Involved in Acute Kidney Injury via Regulating STAT1 Signaling.Journal of immunology research · 2026Article
- Protective effects of S-adenosyl methionine on oxidative stress and tissue damage in STZ-induced diabetic rats.Amino acids · 2025Article
- Bacterial small molecule metabolites implicated in gastrointestinal cancer development.Nature reviews. Microbiology · 2025Review
- Inflammation primes the murine kidney for recovery by activating AZIN1 adenosine-to-inosine editing.The Journal of clinical investigation · 2024Article
- 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
- Inflammation primes the kidney for recovery by activating AZIN1 A-to-I editing.bioRxiv : the preprint server for biology · 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
- 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
- Article
- (The Journal of biological chemistry · 2020Article
- Polyamine Catabolism in Acute Kidney Injury.International journal of molecular sciences · 2019Review
- Distinct patterns of transcriptional and epigenetic alterations characterize acute and chronic kidney injury.Scientific reports · 2018Article
- Polyamine catabolism and oxidative damage.The Journal of biological chemistry · 2018Review
- Endotoxin Preconditioning Reprograms S1 Tubules and Macrophages to Protect the Kidney.Journal of the American Society of Nephrology : JASN · 2018Article
- Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The expression of catabolic enzymes spermidine/spermine N(1)-acetyltransferase (SSAT) and spermine oxidase (SMO) increases after ischemic reperfusion injury. We hypothesized that polyamine catabolism is upregulated and that this increase in catabolic response contributes to tissue damage in endotoxin-induced acute kidney injury (AKI). SSAT mRNA expression peaked at threefold 24 h following LPS injection and returned to background levels by 48 h. The activity of SSAT correlated with its mRNA levels. The expression of SMO also increased in the kidney after LPS administration. Serum creatinine levels increased significantly at approximately 15 h, peaking by 24 h, and returned to background levels by 72 h. To test the role of SSAT in endotoxin-induced AKI, we injected wild-type (SSAT-wt) and SSAT-deficient (SSAT-ko) mice with LPS. Compared with SSAT-wt mice, the SSAT-ko mice subjected to endotoxic-AKI had less severe kidney damage as indicated by better preservation of kidney function. The role of polyamine oxidation in the mediation of kidney injury was examined by comparing the severity of renal damage in SSAT-wt mice treated with MDL72527, an inhibitor of both polyamine oxidase and SMO. Animals treated with MDL72527 showed significant protection against endotoxin-induced AKI. We conclude that increased polyamine catabolism through generation of by-products of polyamine oxidation contributes to kidney damage and that modulation of polyamine catabolism may be a viable approach for the treatment of endotoxin-induced AKI.
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