ArticleInternational journal of molecular sciences2022
Magnesium Isoglycyrrhizinate Reduces the Target-Binding Amount of Cisplatin to Mitochondrial DNA and Renal Injury through SIRT3.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Targeted Sirtuin 3 Activation by Biomimetic Black Phosphorus Nanosheets Mitigates Sepsis-Induced Acute Kidney Injury through Yeast Mitochondrial Escape 1-Like 1 Deacetylation.Biomaterials research · 2026Article
- Licochalcone A mitigates cisplatin-induced nephrotoxicity by inhibiting ferroptosis and mitochondrial dysfunction via the Nrf2/GPX4 axis.Frontiers in pharmacology · 2026Article
- Sirtuin 3 in diabetic kidney disease: mechanisms and pharmacotherapy.Renal failure · 2025Review
- The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Metabolomic and Cellular Mechanisms of Drug-Induced Ototoxicity and Nephrotoxicity: Therapeutic Implications of Uric Acid Modulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Magnesium isoglycyrrhizinate prevented the liver injury of acetaminophen by promoting mitochondrial biogenesis.Toxicology research · 2025Article
- Dexmedetomidine ameliorates hepatic ischemia reperfusion injury via modulating SIRT3 mediated mitochondrial quality control.Scientific reports · 2025Article
- Histone deacetylases: potential therapeutic targets in cisplatin-induced acute kidney injury.Annals of medicine · 2024Review
- PGC-1Acta pharmaceutica Sinica. B · 2024Article
- Magnesium Ion: A New Switch in Tumor Treatment.Biomedicines · 2024Review
- The Role of Mitochondrial Sirtuins (SIRT3, SIRT4 and SIRT5) in Renal Cell Metabolism: Implication for Kidney Diseases.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Nephrotoxicity is the dose-limiting factor of cisplatin treatment. Magnesium isoglycyrrhizinate (MgIG) has been reported to ameliorate renal ischemia-reperfusion injury. This study aimed to investigate the protective effect and possible mechanisms of MgIG against cisplatin-induced nephrotoxicity from the perspective of cellular pharmacokinetics. We found that cisplatin predominantly accumulated in mitochondria of renal tubular epithelial cells, and the amount of binding with mitochondrial DNA (mtDNA) was more than twice that with nuclear DNA (nDNA). MgIG significantly lowered the accumulation of cisplatin in mitochondria and, in particular, the degree of target-binding to mtDNA. MgIG notably ameliorated cisplatin-induced changes in mitochondrial membrane potential, morphology, function, and cell viability, while the magnesium donor drugs failed to work. In a mouse model, MgIG significantly alleviated cisplatin-caused renal dysfunction, pathological changes of renal tubules, mitochondrial ultrastructure variations, and disturbed energy metabolism. Both in vitro and in vivo data showed that MgIG recovered the reduction of NAD
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