Featured Publications
Digoxin Suppresses Pyruvate Kinase M2-Promoted HIF-1α Transactivation in Steatohepatitis
Ouyang X, Han SN, Zhang JY, Dioletis E, Nemeth BT, Pacher P, Feng D, Bataller R, Cabezas J, Stärkel P, Caballeria J, Pongratz RL, Cai SY, Schnabl B, Hoque R, Chen Y, Yang WH, Garcia-Martinez I, Wang FS, Gao B, Torok NJ, Kibbey RG, Mehal WZ. Digoxin Suppresses Pyruvate Kinase M2-Promoted HIF-1α Transactivation in Steatohepatitis. Cell Metabolism 2018, 27: 339-350.e3. PMID: 29414684, PMCID: PMC5806149, DOI: 10.1016/j.cmet.2018.01.007.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCell NucleusChromatinDigoxinDisease Models, AnimalEndotoxinsHistonesHumansHypoxia-Inducible Factor 1, alpha SubunitInflammationLiverNon-alcoholic Fatty Liver DiseaseOxidation-ReductionProtein BindingPyruvate KinaseTHP-1 CellsTranscription, GeneticTranscriptional ActivationConceptsHIF-1α transactivationSterile inflammationHIF-1α pathway activationNon-alcoholic steatohepatitisKinase M2Major clinical consequencesAbility of digoxinLiver inflammationLiver diseasePyruvate kinase M2Clinical consequencesTherapeutic targetInflammationTissue damageHIF-1αPathway activationDigoxinOxidative stressCardiac glycosidesSteatohepatitisDigoxin bindsNovel roleLiverUbiquitous responseActivation
2019
The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer
Wu M, Leng W, Pan H, Lei X, Chen L, Ouyang X, Liang Z. The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer. Mediators Of Inflammation 2019, 2019: 6705424. PMID: 31007603, PMCID: PMC6441532, DOI: 10.1155/2019/6705424.Peer-Reviewed Original ResearchConceptsDiabetic foot ulcersCourse of diseaseInterleukin-6Diabetes mellitusFoot ulcersWound groupChronic diabetic foot ulcersChronic wound groupsReduced expressionUncontrolled chronic inflammationRelevant clinical dataExpression of NFResults of immunofluorescenceChronic inflammationInflammatory pathwaysIntractable complicationClinical dataImmunohistochemical stainingRefractory woundsInflammatory regulationInflammationUlcersPatientsAW groupUncontrolled activation