2021
ATPIF1 maintains normal mitochondrial structure which is impaired by CCM3 deficiency in endothelial cells
Wang K, Chen H, Zhou Z, Zhang H, Zhou HJ, Min W. ATPIF1 maintains normal mitochondrial structure which is impaired by CCM3 deficiency in endothelial cells. Cell & Bioscience 2021, 11: 11. PMID: 33422124, PMCID: PMC7796565, DOI: 10.1186/s13578-020-00514-z.Peer-Reviewed Original ResearchActivation of mitophagyHuman umbilical vein endothelial cellsNormal mitochondrial structureMorphology of mitochondriaRNA-seq screeningMitochondrial membrane potentialCRISPR-Cas9 SystemCerebral cavernous malformationsEndothelial cellsExpression of KLF4Destruction of mitochondriaUmbilical vein endothelial cellsMitochondrial structureSignaling pathwaysVein endothelial cellsMitochondriaATPIF1MitophagyEndothelial progenitor cellsProgenitor cellsCell proliferationMembrane potentialKLF4PathwayProtein
2019
Critical role of Lin28‐TNFR2 signalling in cardiac stem cell activation and differentiation
Xiang Q, Yang B, Li L, Qiu B, Qiu C, Gao X, Zhou H, Min W. Critical role of Lin28‐TNFR2 signalling in cardiac stem cell activation and differentiation. Journal Of Cellular And Molecular Medicine 2019, 23: 0-0. PMID: 30734494, PMCID: PMC6433861, DOI: 10.1111/jcmm.14202.Peer-Reviewed Original ResearchConceptsCardiac stem cell activationStem cell activationHuman inducible pluripotent stem cellsCardiac stem cell differentiationCSC activationStem cell differentiationInducible pluripotent stem cellsPluripotent stem cellsCardiac progenitor cellsCritical roleActivation of TNFR2Factor RNACell activationProtein Lin28Cardiomyocyte proteinsCell differentiationStem cellsProgenitor cellsStem cell-based therapiesCSC differentiationProtein expressionDifferentiationCell-based therapiesExpressionActivation
2017
Smooth muscle cell differentiation: Mechanisms and models for vascular diseases
Deng Y, Lin C, Zhou H, Min W. Smooth muscle cell differentiation: Mechanisms and models for vascular diseases. Frontiers In Biology 2017, 12: 392-405. DOI: 10.1007/s11515-017-1473-z.Peer-Reviewed Original ResearchVSMC differentiationVascular diseaseVSMC behaviorEnvironmental cuesVSMC phenotypeMolecular mechanismsPhenotypic switchingPhenotype modulationMature cellsNew therapeutic targetsSynthetic stateProgenitor cellsSmooth muscle cellsMuscle cellsCritical roleVascular-related diseasesTherapeutic targetDifferentiationCardiovascular diseaseCardiovascular conditionsCellsContractile stateDiseaseComprehensive understandingPhenotype