ArticleInternational journal of molecular sciences2023
Paricalcitol Ameliorates Acute Kidney Injury in Mice by Suppressing Oxidative Stress and Inflammation via Nrf2/HO-1 Signaling.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Ginsenoside Rg1 ameliorates renal ischemia-reperfusion injury by inhibiting FABP1-regulated Nrf2/HO-1 pathway.Renal failure · 2026Article
- Morroniside inJournal of clinical biochemistry and nutrition · 2026Article
- Attenuating amiodarone-induced lung toxicity by the vitamin D receptor activator paricalcitol in rats: targeting TLR4/NF-κB/HIF-1α and TGF-β/Smad signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Therapeutic Effects ofPediatric discovery · 2025Article
- Tanshinone IIA alleviates LPS-induced acute kidney injury by inhibiting RIP3/Nrf2-mediated oxidative stress.Renal failure · 2025Article
- Repurposing mitochondria-targeted therapeutics for kidney diseases.Kidney international · 2025Review
- Preventive and therapeutic effects of cepharanthine on acetaminophen-induced acute liver and kidney injury in male laboratory mice.Gastroenterology and hepatology from bed to bench · 2025Article
- Vitamin D, Cellular Senescence and Chronic Kidney Diseases: What Is Missing in the Equation?Nutrients · 2023Review
- The roles of heme oxygenase-1 in renal disease.Frontiers in nephrology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Effective and targeted prevention and treatment methods for acute kidney injury (AKI), a common clinical complication, still needs to be explored. Paricalcitol is a biologically active chemical that binds to vitamin D receptors in the body to exert anti-oxidant and anti-inflammatory effects. However, the molecular mechanism of the effect of paricalcitol on AKI remains unclear. The current study uses a paricalcitol pretreatment with a mouse AKI model induced by cisplatin to detect changes in renal function, pathology and ultrastructure. Results showed that paricalcitol significantly improved renal function in mice and reduced inflammatory cell infiltration and mitochondrial damage in renal tissue. Furthermore, paricalcitol markedly suppressed reactive oxygen species and malondialdehyde levels in the kidneys of AKI mice and increased the levels of glutathione, superoxide dismutase, Catalase and total anti-oxidant capacity. In addition, we detected renal necrosis and inflammation-related proteins in AKI mice by immunofluorescence and Western blot, and found that their levels were markedly decreased after paricalcitol pretreatment. Moreover, paricalcitol promotes nuclear factor erythroid 2-related factor 2 (
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Registered trials
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