2019
Mitochondrial thioredoxin-2 maintains HCN4 expression and prevents oxidative stress-mediated sick sinus syndrome
Yang B, Huang Y, Zhang H, Huang Y, Zhou HJ, Young L, Xiao H, Min W. Mitochondrial thioredoxin-2 maintains HCN4 expression and prevents oxidative stress-mediated sick sinus syndrome. Journal Of Molecular And Cellular Cardiology 2019, 138: 291-303. PMID: 31751569, DOI: 10.1016/j.yjmcc.2019.10.009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBradycardiaCardiomyopathy, DilatedEnhancer Elements, GeneticHistone DeacetylasesHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMEF2 Transcription FactorsMice, KnockoutMitochondria, HeartModels, BiologicalOxidative StressPhenotypeProtein BindingReactive Oxygen SpeciesRNA, MessengerSick Sinus SyndromeSinoatrial NodeThioredoxinsConceptsSick sinus syndromeSinus syndromeHistone deacetylase 4Lower heart rateHeart rateHCN4 expressionConduction systemSinoatrial nodeNormal heart rateCardiac conduction systemHistone 3 acetylationMitochondrial oxidative stressSinus bradycardiaCardiac functionLox/SyndromeHeart rhythmMyosin heavy chainHistological analysisMiceDeletion miceOxidative stressWhole heartProtein levelsUnderlying mechanism
2015
Autonomic dysfunction independently predicts poor cardiovascular outcomes in asymptomatic individuals with type 2 diabetes in the DIAD study
Chyun DA, Wackers FJ, Inzucchi SE, Jose P, Weiss C, Davey JA, Heller GV, Iskandrian AE, Young LH, Investigators F. Autonomic dysfunction independently predicts poor cardiovascular outcomes in asymptomatic individuals with type 2 diabetes in the DIAD study. SAGE Open Medicine 2015, 3: 2050312114568476. PMID: 26770763, PMCID: PMC4679226, DOI: 10.1177/2050312114568476.Peer-Reviewed Original ResearchCardiac autonomic neuropathyHeart rate ratioAdverse cardiac outcomesHigher pulse pressureAutonomic neuropathyType 2 diabetesCardiac outcomesNon-Black ethnicityHeart rate variabilityInsulin useAsymptomatic individualsPulse pressureCardiac diseaseHeart rateRate ratioGreater systolic blood pressure decreasePower spectral analysisSystolic blood pressure decreaseRate variabilityAsymptomatic Diabetics (DIAD) studyAsymptomatic type 2Composite clinical outcomeHigher glycated hemoglobinPoor cardiac outcomesPoor cardiovascular outcomes
1999
Insulin-like growth factor I stimulates cardiac myosin heavy chain and actin synthesis in the awake rat
Young L, Renfu Y, Hu X, Chong S, Hasan S, Jacob R, Sherwin R. Insulin-like growth factor I stimulates cardiac myosin heavy chain and actin synthesis in the awake rat. American Journal Of Physiology 1999, 276: e143-e150. PMID: 9886960, DOI: 10.1152/ajpendo.1999.276.1.e143.Peer-Reviewed Original ResearchConceptsInsulin-like growth factor IGrowth factor IAwake ratsMyosin heavy chainFactor IContractile protein synthesisIGF-I infusionLow-dose IGFMixed cardiac proteinsCardiac myosin heavy chainMyosin synthesisBlood pressureOvernight fastIntravenous infusionRight ventricleHeavy chainHeart rateHypoglycemic effectFed ratsIGFRatsDirect actionProtein synthesisSalineCardiac proteins