β-Hydroxybutyrate against Cisplatin-Induced acute kidney injury via inhibiting NLRP3 inflammasome and oxidative stress
Authors:
- 5 August 2022
- journal article
- research article
- Published by Elsevier in International Immunopharmacology
- Vol. 111, 109101
Abstract
No abstract availableKeywords
Funding Information
- National Natural Science Foundation of China (81730018)
This publication has 49 references indexed in Scilit:
- The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory diseaseNature Medicine, 2015
- Protection of Hypoglycemia-Induced Neuronal Death by β-Hydroxybutyrate Involves the Preservation of Energy Levels and Decreased Production of Reactive Oxygen SpeciesJournal of Cerebral Blood Flow & Metabolism, 2015
- Sirtuin 3–dependent mitochondrial dynamic improvements protect against acute kidney injuryJournal of Clinical Investigation, 2015
- β-hydroxybutyrate: Much more than a metaboliteDiabetes Research and Clinical Practice, 2014
- Ketone bodies as signaling metabolitesTrends in Endocrinology & Metabolism, 2014
- Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase InhibitorScience, 2013
- p66Shc mediates high-glucose and angiotensin II-induced oxidative stress renal tubular injury via mitochondrial-dependent apoptotic pathwayAmerican Journal of Physiology-Renal Physiology, 2010
- Mechanisms of Cisplatin NephrotoxicityToxins, 2010
- Fuel Metabolism in StarvationAnnual Review of Nutrition, 2006
- β-hydroxybutyrate–induced growth inhibition and collagen production in HK-2 cells are dependent on TGF-β and Smad3Kidney International, 2003