2021
Effects of canagliflozin on human myocardial redox signalling: clinical implications
Kondo H, Akoumianakis I, Badi I, Akawi N, Kotanidis CP, Polkinghorne M, Stadiotti I, Sommariva E, Antonopoulos AS, Carena MC, Oikonomou EK, Reus EM, Sayeed R, Krasopoulos G, Srivastava V, Farid S, Chuaiphichai S, Shirodaria C, Channon KM, Casadei B, Antoniades C. Effects of canagliflozin on human myocardial redox signalling: clinical implications. European Heart Journal 2021, 42: 4947-4960. PMID: 34293101, PMCID: PMC8691807, DOI: 10.1093/eurheartj/ehab420.Peer-Reviewed Original ResearchConceptsNADPH oxidase activityMyocardial redoxHuman cardiomyocytesNOS couplingAtrial tissueSodium-glucose cotransporter 2 inhibitorsMyocardial NADPH oxidase activityRight atrial appendage biopsiesNitric oxide synthase uncouplingCotransporter 2 inhibitorsEffects of canagliflozinHeart failure patientsBeneficial cardiac effectsExpression of inflammationRecent clinical trialsAMP kinaseHuman atrial tissueOxidase activityPrimary human cardiomyocytesAnti-apoptotic effectsTetrahydrobiopterin bioavailabilityCardiovascular outcomesCardiac effectsFailure patientsCardiac surgery
2020
Direct effects of canagliflozin on human myocardial redox signalling: a novel role for SGLT1 inhibition
Kondo H, Akoumianakis I, Akawi N, Kotanidis C, Antonopoulos A, Carena M, Badi I, Oikonomou E, Reus E, Krasopoulos G, Chuaiphichai S, Shirodaria C, Channon K, Casadei B, Antoniades C. Direct effects of canagliflozin on human myocardial redox signalling: a novel role for SGLT1 inhibition. European Heart Journal 2020, 41: ehaa946.3351. DOI: 10.1093/ehjci/ehaa946.3351.Peer-Reviewed Original ResearchHuman primary cardiomyocytesNitric oxide synthaseMyocardial biopsiesHuman myocardial biopsiesMyocardial redoxOxide synthaseHuman myocardiumSodium-glucose cotransporter 2 inhibitorsMyocardial NADPH oxidase activityRight atrial appendage biopsiesGlucose cotransporter 2 inhibitorsUncoupled nitric oxide synthaseSGLT1/SGLT2 inhibitorsCotransporter 2 inhibitorsEffects of canagliflozinHeart failure patientsPro-fibrotic markersRecent clinical trialsBritish Heart FoundationNADPH oxidase subunitsBioavailability of tetrahydrobiopterinNADPH oxidase activityAnti-apoptotic effectsDirect effectBasal O2Insulin-induced vascular redox dysregulation in human atherosclerosis is ameliorated by dipeptidyl peptidase 4 inhibition
Akoumianakis I, Badi I, Douglas G, Chuaiphichai S, Herdman L, Akawi N, Margaritis M, Antonopoulos AS, Oikonomou EK, Psarros C, Galiatsatos N, Tousoulis D, Kardos A, Sayeed R, Krasopoulos G, Petrou M, Schwahn U, Wohlfart P, Tennagels N, Channon KM, Antoniades C. Insulin-induced vascular redox dysregulation in human atherosclerosis is ameliorated by dipeptidyl peptidase 4 inhibition. Science Translational Medicine 2020, 12 PMID: 32350133, PMCID: PMC7212010, DOI: 10.1126/scitranslmed.aav8824.Peer-Reviewed Original ResearchConceptsDipeptidyl peptidase-4 inhibitorsCoronary artery bypass surgeryAggressive insulin treatmentInsulin treatmentCoronary atherosclerosisEndothelial functionAbnormal responseHigh-fat diet-fed ApoEOral dipeptidyl peptidase-4 inhibitorLong-term combination therapyHuman internal mammary arteryDipeptidyl peptidase-4 inhibitionHigher cardiac mortalityPeptidase-4 inhibitionVascular insulin responsesVascular redox stateArtery bypass surgeryInternal mammary arteryInsulin resistance statusNitric oxide bioavailabilityPeptidase-4 inhibitorsPlasma DPP4 activityVascular oxidative stressRecent clinical trialsInsulin-sensitizing effects