2021
Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation
Sewanan LR, Park J, Rynkiewicz MJ, Racca AW, Papoutsidakis N, Schwan J, Jacoby DL, Moore JR, Lehman W, Qyang Y, Campbell SG. Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation. The Journal Of General Physiology 2021, 153: e202012640. PMID: 34319370, PMCID: PMC8321830, DOI: 10.1085/jgp.202012640.Peer-Reviewed Original ResearchConceptsHypertrophic cardiomyopathyHeart tissueCellular hypertrophyEngineered Heart TissuePathological cardiac hypertrophyThin filament mutationsMavacamten treatmentDiastolic dysfunctionDisease featuresHypertrophic effectCardiac hypertrophyContractile differencesHypertrophyFundamental disease mechanismsCrossbridge activityInherited disorderOverall Ca2Uncertain significancePatient phenotypesDisease mechanismsLow Ca2PatientsK mutationMavacamtenTissue
2019
Modular design of a tissue engineered pulsatile conduit using human induced pluripotent stem cell-derived cardiomyocytes
Park J, Anderson CW, Sewanan LR, Kural MH, Huang Y, Luo J, Gui L, Riaz M, Lopez CA, Ng R, Das SK, Wang J, Niklason L, Campbell SG, Qyang Y. Modular design of a tissue engineered pulsatile conduit using human induced pluripotent stem cell-derived cardiomyocytes. Acta Biomaterialia 2019, 102: 220-230. PMID: 31634626, PMCID: PMC7227659, DOI: 10.1016/j.actbio.2019.10.019.Peer-Reviewed Original ResearchConceptsSingle-ventricle cardiac defectsHuman umbilical arteryPluripotent stem cell-derived cardiomyocytesStem cell-derived cardiomyocytesFontan procedureSurgical interventionSVD patientsCell-derived cardiomyocytesFontan conduitTherapeutic potentialEngineered Heart TissueVascular conduitsCongenital disorderDesign strategyVariety of complicationsEfficient electrical conductivitySingle ventricle heartPrimary cardiac fibroblastsFontan circulationHeart failureCorrective surgeryUmbilical arteryPulmonary circulationBiodegradable materialsPulmonary system