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 1Enhanced hypoxic tolerance by Seabuckthorn is due to upregulation of HIF-1α and attenuation of ER stress
Jain K, Suryakumar G, Prasad R, Ganju L, Singh S. Enhanced hypoxic tolerance by Seabuckthorn is due to upregulation of HIF-1α and attenuation of ER stress. Journal Of Applied Biomedicine 2016, 14: 71-83. DOI: 10.1016/j.jab.2015.10.001.Peer-Reviewed Original ResearchHIF-1αHypoxic toleranceER stressAnti-inflammatory effectsPro-survival effectsFree radical productionCardioprotective actionCardiac damageHO-1NF-κBHerbal supplementsKey adaptive responseOxidative stressTwo-fold increaseHsp70 levelsAntioxidant potentialProtein carbonylationRadical productionHypoxiaSignificant declineSignaling cascadesAdaptive responseCross talkNovel insightsRedox homeostasis