about
Prevention of postischemic myocardial reperfusion injury by the combined treatment of NCX-4016 and TempolStem cell therapy with overexpressed VEGF and PDGF genes improves cardiac function in a rat infarct modelOxygen-sensitive outcomes and gene expression in acute ischemic strokeHypoxic preconditioning induces the expression of prosurvival and proangiogenic markers in mesenchymal stem cells.Myeloid-derived suppressor cell inhibition of the IFN response in tumor-bearing mice.Amelioration of doxorubicin-induced cardiotoxicity by an anticancer-antioxidant dual-function compound, HO-3867Mesenchymal stem cells for cardiac regeneration: translation to bedside realityRole of oxygen in postischemic myocardial injury.Sivelestat attenuates myocardial reperfusion injury during brief low flow postischemic infusion.Cardioprotection by HO-4038, a novel verapamil derivative, targeted against ischemia and reperfusion-mediated acute myocardial infarctionPulmonary hypertension secondary to left-heart failure involves peroxynitrite-induced downregulation of PTEN in the lung.Myocardial oxygenation and functional recovery in infarct rat hearts transplanted with mesenchymal stem cellsHyperbaric oxygenation enhances transplanted cell graft and functional recovery in the infarct heartIntermittent hypoxia exacerbates pancreatic β-cell dysfunction in a mouse model of diabetes mellitusChronic heart failure and the substrate for atrial fibrillation.Oxygen and oxygenation in stem-cell therapy for myocardial infarctionStem cell transplantation as a therapy for cardiac fibrosis.Emerging role of oxidative stress in metabolic syndrome and cardiovascular diseases: important role of Rac/NADPH oxidase.Selective inhibition of hypoxia-inducible factor 1α ameliorates adipose tissue dysfunction.Oxygen cycling in conjunction with stem cell transplantation induces NOS3 expression leading to attenuation of fibrosis and improved cardiac functionDysregulation of PTEN in cardiopulmonary vascular remodeling induced by pulmonary hypertension.p53's choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.Crataegus oxycantha extract attenuates apoptotic incidence in myocardial ischemia-reperfusion injury by regulating Akt and HIF-1 signaling pathways.Pharmacological preconditioning of mesenchymal stem cells with trimetazidine (1-[2,3,4-trimethoxybenzyl]piperazine) protects hypoxic cells against oxidative stress and enhances recovery of myocardial function in infarcted heart through Bcl-2 expressPotential Role of Exosomes in Mending a Broken Heart: Nanoshuttles Propelling Future Clinical Therapeutics Forward.C-phycocyanin protects against ischemia-reperfusion injury of heart through involvement of p38 MAPK and ERK signaling.C-phycocyanin ameliorates doxorubicin-induced oxidative stress and apoptosis in adult rat cardiomyocytes.Labeling of skeletal myoblasts with a novel oxygen-sensing spin probe for noninvasive monitoring of in situ oxygenation and cell therapy in heart.Spirulina attenuates cyclosporine-induced nephrotoxicity in rats.Protection against cisplatin-induced nephrotoxicity by Spirulina in rats.Skeletal myoblasts transplanted in the ischemic myocardium enhance in situ oxygenation and recovery of contractile function.Cardiac remodeling caused by transgenic overexpression of a corn Rac gene.N-hydroxy-pyrroline modification of verapamil exhibits antioxidant protection of the heart against ischemia/reperfusion-induced cardiac dysfunction without compromising its calcium antagonistic activityCardioprotection by sulfaphenazole, a cytochrome p450 inhibitor: mitigation of ischemia-reperfusion injury by scavenging of reactive oxygen speciesStructure-activity studies on the protection of Trimetazidine derivatives modified with nitroxides and their precursors from myocardial ischemia-reperfusion injuryEffect of pulmonary-generated reactive oxygen species on left-ventricular dysfunction associated with cardio-pulmonary ischemia-reperfusion injuryMyocardial Rac1 exhibits partial involvement in thyroxin-induced cardiomyocyte hypertrophy and its inhibition is not sufficient to improve cardiac dysfunction or contractile abnormalities in mouse papillary musclesCurrent research trends and challenges in tissue engineering for mending broken hearts
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description
researcher ORCID ID = 0000-0003-3430-374X
@en
wetenschapper
@nl
name
Mahmood Khan
@ast
Mahmood Khan
@en
Mahmood Khan
@es
Mahmood Khan
@nl
type
label
Mahmood Khan
@ast
Mahmood Khan
@en
Mahmood Khan
@es
Mahmood Khan
@nl
prefLabel
Mahmood Khan
@ast
Mahmood Khan
@en
Mahmood Khan
@es
Mahmood Khan
@nl
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P1153
7410318160
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0000-0003-3430-374X