Stuart Campbell
ProfessorCards
About
Research
Publications
2025
Evaluating pathogenicity of TPM1 variants of unknown significance using in-silico and in-vitro models
Halder S, Bellitto J, Rynkiewicz M, Cheung F, Liu D, Firlar I, Bongiorno A, Barry M, Sewanan L, Moore J, Lehman W, Campbell S. Evaluating pathogenicity of TPM1 variants of unknown significance using in-silico and in-vitro models. The Journal Of Precision Medicine Health And Disease 2025, 2: 100008. DOI: 10.1016/j.premed.2025.100008.Peer-Reviewed Original ResearchIn vitro motilityFilament motilityContext of cardiomyopathyVariant classificationGenetic screeningTwitch contraction forceComputational pipelineMyosin activityEvaluate pathogenicityDiversity changesFunctional studiesIn silicoTropomyosinTPM1VUSMotilityInherited cardiomyopathyCa2+ sensitivityVariantsIn vitro modelIn vitro dataReduced abilityIPSC-derived cardiomyocytesLow Ca2+Ca2+Application of instant assembly of collagen to bioprint cardiac tissues
Xiao H, Liang Z, Gong X, Jordan S, Rossello-Martinez A, Gokhan I, Li X, Wen Z, Lee S, Campbell S, Qyang Y, Mak M. Application of instant assembly of collagen to bioprint cardiac tissues. APL Bioengineering 2025, 9: 026124. PMID: 40520649, PMCID: PMC12165719, DOI: 10.1063/5.0252746.Peer-Reviewed Original ResearchScreening single nucleotide changes to tropomyosin to identify novel cardiomyopathy mutants
Wen J, Campbell S, Moore J, Lehman W, Rynkiewicz M. Screening single nucleotide changes to tropomyosin to identify novel cardiomyopathy mutants. Journal Of Molecular And Cellular Cardiology 2025, 203: 82-90. PMID: 40268117, PMCID: PMC12135046, DOI: 10.1016/j.yjmcc.2025.04.009.Peer-Reviewed Original ResearchConceptsDeleterious effects of mutationsTropomyosin-actin interactionsSingle nucleotide mutationsEffects of mutationsThin filament regulationDilated cardiomyopathyTropomyosin sequencesActin interactionNucleotide mutationsFilament regulationMutation-sensitiveSubcellular unitsMutantsPathological cardiac remodelingTropomyosinActinThin filamentsEarly therapeutic interventionFunctional analysisMutationsInherited cardiomyopathyCardiac remodelingCardiac functionRegulatory BCardiomyopathyINHIBITION OF THE PI3K-AKT SIGNALING PATHWAY REVERSES HYPERTROPHY OF HUMAN INDUCED PLURIPOTENT STEM CELL-DERIVED CARDIOMYOCYTES MODELING HYPERTROPHIC CARDIOMYOPATHY
Zanetti M, Agashe R, Sewanan L, Li X, Campbell S, Shimada Y. INHIBITION OF THE PI3K-AKT SIGNALING PATHWAY REVERSES HYPERTROPHY OF HUMAN INDUCED PLURIPOTENT STEM CELL-DERIVED CARDIOMYOCYTES MODELING HYPERTROPHIC CARDIOMYOPATHY. Journal Of The American College Of Cardiology 2025, 85: 1360. DOI: 10.1016/s0735-1097(25)01844-3.Peer-Reviewed Original ResearchBPS2025 - R451G desmoplakin induces contractile deficits in engineered heart tissue
Gokhan I, Pagan A, Campbell S. BPS2025 - R451G desmoplakin induces contractile deficits in engineered heart tissue. Biophysical Journal 2025, 124: 616a. DOI: 10.1016/j.bpj.2024.11.3180.Peer-Reviewed Original Research
2024
Distinct mechanisms drive divergent phenotypes in hypertrophic and dilated cardiomyopathy associated TPM1 variants
Halder S, Rynkiewicz M, Kim L, Barry M, Zied A, Sewanan L, Kirk J, Moore J, Lehman W, Campbell S. Distinct mechanisms drive divergent phenotypes in hypertrophic and dilated cardiomyopathy associated TPM1 variants. Journal Of Clinical Investigation 2024, 134: e179135. PMID: 39436707, PMCID: PMC11645150, DOI: 10.1172/jci179135.Peer-Reviewed Original ResearchTPM1 mutationActin thin filamentsDilated cardiomyopathyE54KPhenotypic diversityMyosin activityStem cell-derived cardiomyocytesGene expressionHuman engineered heart tissueIncreased calcium sensitivitySarcomeric proteinsCell-derived cardiomyocytesThin filamentsK mutationMolecular eventsTPM1MutationsClinical phenotypePhenotypeAllosteric interactionsGenesMuscle contractilityCalcium sensitivityInherited disorderAssociation rateIn silico and in vitro models reveal the molecular mechanisms of hypocontractility caused by TPM1 M8R
Creso J, Gokhan I, Rynkiewicz M, Lehman W, Moore J, Campbell S. In silico and in vitro models reveal the molecular mechanisms of hypocontractility caused by TPM1 M8R. Frontiers In Physiology 2024, 15: 1452509. PMID: 39282088, PMCID: PMC11392859, DOI: 10.3389/fphys.2024.1452509.Peer-Reviewed Original ResearchDilated cardiomyopathyManifestation of dilated cardiomyopathyTropomyosin-actin interactionsIntact cardiac muscleIsometric twitch forceCardiac muscle disordersSevere heart failureHuman engineered heart tissueGenotype-phenotype relationshipsDose-dependent mannerDuration of contractionIn silico predictionIn vitro modelDepressed contractilityMutant tissueCardiac sarcomereLinkage studiesHeart failureTropomyosin chainTwitch contractionsCardiac thin filamentsInherited disorderMuscle disordersMutation pathogenicityCardiac muscleEngineered heart tissue: Design considerations and the state of the art
Gokhan I, Blum T, Campbell S. Engineered heart tissue: Design considerations and the state of the art. Biophysics Reviews 2024, 5: 021308. PMID: 38912258, PMCID: PMC11192576, DOI: 10.1063/5.0202724.Peer-Reviewed Original ResearchContractile phenotypes of engineered heart tissues derived from hypertrophic cardiomyopathy patients lacking sarcomeric mutations
Rasheed Y, Young S, Halder S, Li X, Stendahl J, Campbell S. Contractile phenotypes of engineered heart tissues derived from hypertrophic cardiomyopathy patients lacking sarcomeric mutations. Biophysical Journal 2024, 123: 388a. DOI: 10.1016/j.bpj.2023.11.2357.Peer-Reviewed Original ResearchDifferent mechanistic and molecular cues modulate divergent phenotypes in HCM and DCM mutations to TPM1
Halder S, Rynkiewicz M, Moore J, Lehman W, Campbell S. Different mechanistic and molecular cues modulate divergent phenotypes in HCM and DCM mutations to TPM1. Biophysical Journal 2024, 123: 18a. DOI: 10.1016/j.bpj.2023.11.222.Peer-Reviewed Original Research