Oxidative injury is a common consequence of BMPR2 mutations.
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Redox biology in pulmonary arterial hypertension (2013 Grover Conference Series)BMPR2 spruces up the endothelium in pulmonary hypertensionThe adventitia: essential regulator of vascular wall structure and functionRole of oxidized lipids in pulmonary arterial hypertensionDysfunctional BMPR2 signaling drives an abnormal endothelial requirement for glutamine in pulmonary arterial hypertensionInteraction between bone morphogenetic protein receptor type 2 and estrogenic compounds in pulmonary arterial hypertensionIdentification of a common Wnt-associated genetic signature across multiple cell types in pulmonary arterial hypertension.Physiologic and molecular consequences of endothelial Bmpr2 mutation.BMP pathway regulation of and by macrophages.BMPR2 preserves mitochondrial function and DNA during reoxygenation to promote endothelial cell survival and reverse pulmonary hypertensionRescuing the BMPR2 signaling axis in pulmonary arterial hypertensionIdiopathic and heritable PAH perturb common molecular pathways, correlated with increased MSX1 expression.Cytoskeletal defects in Bmpr2-associated pulmonary arterial hypertensionSerotonin 2B Receptor Antagonism Prevents Heritable Pulmonary Arterial Hypertension.Increased Mutagen Sensitivity and DNA Damage in Pulmonary Arterial Hypertension.Metabolomic analysis of bone morphogenetic protein receptor type 2 mutations in human pulmonary endothelium reveals widespread metabolic reprogramming.Connectivity map analysis of nonsense-mediated decay-positive BMPR2-related hereditary pulmonary arterial hypertension provides insights into disease penetrance.Bone morphogenetic protein receptor type II deficiency and increased inflammatory cytokine production. A gateway to pulmonary arterial hypertensionExpression of mutant bone morphogenetic protein receptor II worsens pulmonary hypertension secondary to pulmonary fibrosis.Antagonism of the thromboxane-prostanoid receptor is cardioprotective against right ventricular pressure overload.A potential role for insulin resistance in experimental pulmonary hypertensionHyperoxia synergizes with mutant bone morphogenic protein receptor 2 to cause metabolic stress, oxidant injury, and pulmonary hypertension.A process-based review of mouse models of pulmonary hypertension.Novel serum biomarkers in pulmonary arterial hypertension.Accumulation of isolevuglandin-modified protein in normal and fibrotic lung.Oestrogen inhibition reverses pulmonary arterial hypertension and associated metabolic defects.Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension.Oxidative stress increases M1dG, a major peroxidation-derived DNA adduct, in mitochondrial DNA.Bone morphogenetic protein signaling is required for RAD51-mediated maintenance of genome integrity in vascular endothelial cellsPulmonary Hypertension Is a Probable NO/ONOO− Cycle Disease: A Review
P2860
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P2860
Oxidative injury is a common consequence of BMPR2 mutations.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Oxidative injury is a common consequence of BMPR2 mutations.
@en
type
label
Oxidative injury is a common consequence of BMPR2 mutations.
@en
prefLabel
Oxidative injury is a common consequence of BMPR2 mutations.
@en
P2093
P2860
P356
P1476
Oxidative injury is a common consequence of BMPR2 mutations.
@en
P2093
Anna R Hemnes
Candice Fike
Eric Austin
James West
Jennifer A Johnson
Joshua P Fessel
Kirk L Lane
L Jackson Roberts
Linda Robinson
Megha Talati
P2860
P356
10.4103/2045-8932.78107
P577
2011-01-01T00:00:00Z