2021
Honokiol regulates mitochondrial substrate utilization and cellular fatty acid metabolism in diabetic mice heart
Jayakumari N, Rajendran R, Sivasailam A, Parambil S, Reghuvaran A, Sreelatha H, Gopala S. Honokiol regulates mitochondrial substrate utilization and cellular fatty acid metabolism in diabetic mice heart. European Journal Of Pharmacology 2021, 896: 173918. PMID: 33529726, DOI: 10.1016/j.ejphar.2021.173918.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAMP-Activated Protein KinasesAnimalsAntioxidantsBiphenyl CompoundsCD36 AntigensDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Energy MetabolismFatty AcidsLignansMaleMice, Inbred C57BLMitochondria, HeartMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR alphaStreptozocinSuperoxide DismutaseConceptsComplex IFatty acid metabolismMitochondrial metabolic changesAcetylation/deacetylation mechanismCellular fatty acid metabolismFatty acid respirationAcid metabolismHonokiol treatmentMitochondrial substrate utilizationMouse cardiac mitochondriaCardiac mitochondriaType 2 diabetes mellitusNuclear transcription factorPeroxisome proliferator-activated receptor αProtein functionProliferator-activated receptor αAcetylated proteinsTranscription factorsDiabetic mouse heartsCardiac mitochondrial dysfunctionCardiac mitochondrial functionDeacetylation mechanismExpression of clusterMitochondrial functionMitochondrial dysfunction
2014
High fat, high sucrose diet causes cardiac mitochondrial dysfunction due in part to oxidative post-translational modification of mitochondrial complex II
Sverdlov AL, Elezaby A, Behring JB, Bachschmid MM, Luptak I, Tu VH, Siwik DA, Miller EJ, Liesa M, Shirihai OS, Pimentel DR, Cohen RA, Colucci WS. High fat, high sucrose diet causes cardiac mitochondrial dysfunction due in part to oxidative post-translational modification of mitochondrial complex II. Journal Of Molecular And Cellular Cardiology 2014, 78: 165-173. PMID: 25109264, PMCID: PMC4268348, DOI: 10.1016/j.yjmcc.2014.07.018.Peer-Reviewed Original ResearchConceptsCysteine oxidative post-translational modificationsOxidative post-translational modificationsCardiac mitochondrial proteinsPost-translational modificationsMetabolic heart diseaseMitochondrial proteinsATP synthesisMitochondrial dysfunctionBasic Mitochondrial BiologyCardiac mitochondriaMitochondrial biologyOxidative stressTag labelingCardiac mitochondrial dysfunctionBiotin switchSubunit AATP productionMitochondrial ROSGSH/GSSG ratioFunctional consequencesMitochondriaReversible oxidationGSSG ratioProteinSDHA
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