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
2023
SOD2 in platelets: with age comes responsibility
Jain K, Gu S, Hwa J. SOD2 in platelets: with age comes responsibility. Journal Of Thrombosis And Haemostasis 2023, 21: 1077-1081. PMID: 36716965, DOI: 10.1016/j.jtha.2023.01.016.Peer-Reviewed Original Research
2020
“CO”ping With a Sticky Situation
Jain K, Tyagi T, Hwa J. “CO”ping With a Sticky Situation. Arteriosclerosis Thrombosis And Vascular Biology 2020, 40: 2344-2345. PMID: 32966131, PMCID: PMC7517721, DOI: 10.1161/atvbaha.120.315158.Commentaries, Editorials and Letters
2019
Mitochondrial MsrB2 serves as a switch and transducer for mitophagy
Lee SH, Lee S, Du J, Jain K, Ding M, Kadado AJ, Atteya G, Jaji Z, Tyagi T, Kim W, Herzog RI, Patel A, Ionescu CN, Martin KA, Hwa J. Mitochondrial MsrB2 serves as a switch and transducer for mitophagy. EMBO Molecular Medicine 2019, 11: emmm201910409. PMID: 31282614, PMCID: PMC6685081, DOI: 10.15252/emmm.201910409.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood PlateletsCell LineDiabetes MellitusFemaleHumansMethionine Sulfoxide ReductasesMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsMicrotubule-Associated ProteinsMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitophagyMutationOxidation-ReductionOxidative StressParkinson DiseaseSignal TransductionUbiquitin-Protein LigasesUbiquitinationConceptsReduced mitophagyOxidative stress-induced mitophagyNovel regulatory mechanismStress-induced mitophagyLC3 interactionMitochondrial matrixDamaged mitochondriaMsrB2Reactive oxygen speciesRegulatory mechanismsMethionine oxidationMitophagyMitochondriaPlatelet apoptosisOxygen speciesPlatelet-specific knockoutApoptosisPathophysiological importanceExpressionImportant roleUbiquitinationParkin mutationsParkinSpeciesLC3
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
Upregulation of Cytoprotective Defense Mechanisms and Hypoxia-Responsive Proteins Imparts Tolerance to Acute Hypobaric Hypoxia
Jain K, Suryakumar G, Prasad R, Ganju L. Upregulation of Cytoprotective Defense Mechanisms and Hypoxia-Responsive Proteins Imparts Tolerance to Acute Hypobaric Hypoxia. High Altitude Medicine & Biology 2013, 14: 65-77. PMID: 23537263, DOI: 10.1089/ham.2012.1064.Peer-Reviewed Original ResearchMeSH KeywordsAltitudeAnimalsAtmospheric PressureCatalaseCreatine Kinase, MB FormDyspneaEndothelin-1ErythropoietinHeme Oxygenase-1HSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMaleMalondialdehydeMyocarditisMyocardiumNitric OxideOxidative StressProtein CarbonylationRatsRats, Sprague-DawleyReactive Oxygen SpeciesSuperoxide DismutaseTime FactorsUp-RegulationVascular Endothelial Growth Factor AConceptsEnvironmental stressHypoxia-responsive proteinsSubsequent oxidative damageReactive oxygen species levelsCellular machineryHypoxia-responsive moleculesResponsive genesOxygen species levelsSpecies levelDifferential expressionTolerant animalsDefense mechanismsOxidative damageCytoprotective chaperoneAntioxidant enzymesHypobaric hypoxiaHigh expressionHIF-1αProteinAdult Sprague-Dawley ratsExpressionMyocardial antioxidant enzymesAcute hypobaric hypoxiaSprague-Dawley ratsCK-MB activity