Featured Publications
Age associated non-linear regulation of redox homeostasis in the anucleate platelet: Implications for CVD risk patients
Jain K, Tyagi T, Patell K, Xie Y, Kadado AJ, Lee SH, Yarovinsky T, Du J, Hwang J, Martin KA, Testani J, Ionescu CN, Hwa J. Age associated non-linear regulation of redox homeostasis in the anucleate platelet: Implications for CVD risk patients. EBioMedicine 2019, 44: 28-40. PMID: 31130473, PMCID: PMC6604369, DOI: 10.1016/j.ebiom.2019.05.022.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAge FactorsAgedAged, 80 and overAgingAnimalsAntioxidantsApoptosisBiomarkersBlood PlateletsCardiovascular DiseasesComorbidityDisease Models, AnimalFemaleHomeostasisHumansMaleMiceMiddle AgedOxidation-ReductionOxidative StressPlatelet ActivationPlatelet AdhesivenessReactive Oxygen SpeciesRisk AssessmentRisk FactorsConceptsRisk patientsMouse studiesPlatelet phenotypeMajor adverse cardiovascular eventsHigh cardiovascular risk patientsAdaptive increaseAdverse cardiovascular eventsCentral pathophysiological roleCVD risk patientsCardiovascular risk patientsAggressive antiplatelet therapyEffect of comorbidityAge group 40Young healthy subjectsAntiplatelet therapyCardiovascular eventsYear age cohortAdvanced ageCVD patientsGroup 40Healthy subjectsPathophysiological roleElderly populationCardiovascular pathologyPatients
2016
Amelioration of ER stress by 4-phenylbutyric acid reduces chronic hypoxia induced cardiac damage and improves hypoxic tolerance through upregulation of HIF-1α
Jain K, Suryakumar G, Ganju L, Singh SB. Amelioration of ER stress by 4-phenylbutyric acid reduces chronic hypoxia induced cardiac damage and improves hypoxic tolerance through upregulation of HIF-1α. Vascular Pharmacology 2016, 83: 36-46. PMID: 27058435, DOI: 10.1016/j.vph.2016.03.004.Peer-Reviewed Original ResearchMeSH KeywordsAltitudeAnimalsApoptosisApoptosis Regulatory ProteinsChronic DiseaseCytoprotectionDisease Models, AnimalEndoplasmic Reticulum StressHypertrophy, Right VentricularHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMaleMolecular ChaperonesMyocardiumOxidative StressPhenylbutyratesProtein CarbonylationProteolysisRats, Sprague-DawleySignal TransductionTime FactorsUnfolded Protein ResponseUp-RegulationConceptsChronic hypoxiaHIF-1αCardiac damageUnfolded protein responseER stressHypoxic toleranceRight ventricular enlargementExposure of ratsHypoxia-inducible factor-1ER stress modulationEndoplasmic reticulum stressInducible factor-1Ventricular enlargementCardiac injuryCardioprotective actionCardiovascular diseaseCardiac hypertrophyMarked upregulationActivation of UPRUnderlying causeUPR markersHypoxiaReticulum stressConcomitant suppressionFactor 1
2013
Myocardial ER chaperone activation and protein degradation occurs due to synergistic, not individual, cold and hypoxic stress
Jain K, Suryakumar G, Prasad R, Singh SN, Ganju L. Myocardial ER chaperone activation and protein degradation occurs due to synergistic, not individual, cold and hypoxic stress. Biochimie 2013, 95: 1897-1908. PMID: 23816873, DOI: 10.1016/j.biochi.2013.06.018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCold TemperatureEndoplasmic Reticulum StressGene Expression RegulationHeat-Shock ProteinsHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLipid PeroxidationMaleMyocardiumOxidation-ReductionProteasome Endopeptidase ComplexProtein CarbonylationProtein Disulfide-IsomerasesProtein FoldingProteolysisRatsRats, Sprague-DawleyTranscription Factor CHOPTunicamycinConceptsStress responseHypoxic stressCellular stress responseCell survival kinasesProtein oxidationEndoplasmic reticulum stress responseER stress responseER stress inducersReticulum stress responseMyocardial protein oxidationER chaperone GRP78Chaperone activationMisfolded proteinsEnvironmental stressProtein degradationChaperone GRP78Cold stressSurvival kinasesProtein oxidative modificationStress inducersHigh altitude stressMolecular levelCHOP expressionMatrix remodelingProtein