2016
ISL1 cardiovascular progenitor cells for cardiac repair after myocardial infarction
Bartulos O, Zhuang ZW, Huang Y, Mikush N, Suh C, Bregasi A, Wang L, Chang W, Krause DS, Young LH, Pober JS, Qyang Y. ISL1 cardiovascular progenitor cells for cardiac repair after myocardial infarction. JCI Insight 2016, 1: e80920. PMID: 27525311, PMCID: PMC4982472, DOI: 10.1172/jci.insight.80920.Peer-Reviewed Original ResearchMyocardial infarctionControl animalsCardiovascular progenitor cellsProgenitor cellsVentricular contractile functionCardiac repair strategiesNew blood vesselsInfarct areaLineage-tracing studiesContractile functionCardiac repairBlood vessel formationMyocardial regenerationEndothelial cellsHeart tissueBlood vesselsMurine heartInfarctionVessel formationInjuryMiceDelivery approachCardiomyocytesHeartCells
2011
A small molecule AMPK activator protects the heart against ischemia–reperfusion injury
Kim AS, Miller EJ, Wright TM, Li J, Qi D, Atsina K, Zaha V, Sakamoto K, Young LH. A small molecule AMPK activator protects the heart against ischemia–reperfusion injury. Journal Of Molecular And Cellular Cardiology 2011, 51: 24-32. PMID: 21402077, PMCID: PMC4005884, DOI: 10.1016/j.yjmcc.2011.03.003.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAMP-Activated Protein KinasesAnimalsApoptosisBiphenyl CompoundsCardiotonic AgentsEnzyme ActivatorsHeartIschemic PreconditioningMiceMice, Inbred C57BLMice, TransgenicMyocardial InfarctionMyocardial Reperfusion InjuryNecrosisNitric Oxide Synthase Type IIIPeptide Elongation Factor 2PyronesThiophenesConceptsIschemia-reperfusion injuryLeft ventricular contractile functionMyocardial ischemia-reperfusion injuryMouse heartsEndothelial nitric oxide synthase activationNitric oxide synthase activationLess myocardial necrosisCoronary artery occlusionIschemia-reperfusion damageVentricular contractile functionEukaryotic elongation factor 2Isolated mouse heartsPost-ischemic reperfusionAMPK activatorArtery occlusionIschemic contractureIschemic injuryInfarct sizeMyocardial stunningMyocardial necrosisCardioprotective mechanismsContractile functionSolid organsTherapeutic targetMyocardial apoptosis