Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization. - Wikidata - awgldk - TriplyDB

Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.

Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.

http://www.wikidata.org/entity/Q41824496

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Early injury of the neonatal lung contributes to premature lung aging: a hypothesis Aberrant Pulmonary Vascular Growth and Remodeling in Bronchopulmonary Dysplasia Pathogenesis of bronchopulmonary dysplasia: when inflammation meets organ development Understanding the Impact of Infection, Inflammation, and Their Persistence in the Pathogenesis of Bronchopulmonary Dysplasia Unique aspects of the developing lung circulation: structural development and regulation of vasomotor tone Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia Chronic lung disease in the preterm infant. Lessons learned from animal models Sustained hyperoxia-induced NF-κB activation improves survival and preserves lung development in neonatal mice.Disrupted lung development and bronchopulmonary dysplasia: opportunities for lung repair and regeneration.Vascular mediators in chronic lung disease of infancy: role of endothelial monocyte activating polypeptide II (EMAP II).Bronchopulmonary dysplasia early changes leading to long-term consequences.HIF-1α Plays a Critical Role in the Gestational Sidestream Smoke-Induced Bronchopulmonary Dysplasia in Mice.Resident Endothelial Cells and Endothelial Progenitor Cells Restore Endothelial Barrier Function After Inflammatory Lung Injury.Activation of the nuclear factor-κB pathway during postnatal lung inflammation preserves alveolarization by suppressing macrophage inflammatory protein-2.Type IV collagen drives alveolar epithelial-endothelial association and the morphogenetic movements of septation.Neonatal mice genetically modified to express the elastase inhibitor elafin are protected against the adverse effects of mechanical ventilation on lung growth Small molecular modulation of macrophage migration inhibitory factor in the hyperoxia-induced mouse model of bronchopulmonary dysplasia.Absence of TNF-α enhances inflammatory response in the newborn lung undergoing mechanical ventilation.A20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF-κB activation under hypoxia Epithelial-Derived Inflammation Disrupts Elastin Assembly and Alters Saccular Stage Lung Development Peptides genetically selected for NF-κB activation cooperate with oncogene Ras and model carcinogenic role of inflammation.IκBβ-mediated NF-κB activation confers protection against hyperoxic lung injury.Recent advances in late lung development and the pathogenesis of bronchopulmonary dysplasia.Nuclear factor-kappa-B signaling in lung development and disease: one pathway, numerous functions.A critical review of the American Journal of Physiology-Lung Cellular and Molecular Physiology: 2012-2015.Bronchopulmonary dysplasia - an overview about pathophysiologic concepts.The genome-wide transcriptional response to neonatal hyperoxia identifies Ahr as a key regulator.Perinatal Endotoxemia Induces Sustained Hepatic COX-2 Expression through an NFκB-Dependent Mechanism.Sex-specific differences in neonatal hyperoxic lung injury The BPD trio? Interaction of dysregulated PDGF, VEGF, and TGF signaling in neonatal chronic lung disease.Differential sex-specific effects of oxygen toxicity in human umbilical vein endothelial cells.Oxidative stress diseases unique to the perinatal period: A window into the developing innate immune response.Inhibition of IκBβ/NFκB signaling prevents LPS-induced IL1β expression without increasing apoptosis in the developing mouse lung.Can We Understand the Pathobiology of Bronchopulmonary Dysplasia?Impaired alveolarization and intra-uterine growth restriction in rats: a postnatal genome-wide analysis.Role of LTBP4 in alveolarization, angiogenesis, and fibrosis in lungs.Developmental Differences in Focal Adhesion Kinase Expression Modulate Pulmonary Endothelial Barrier Function in Response to Inflammation.Bacillus Calmette-Guerín vaccination: a novel therapeutic approach to preventing hyperoxic lung injury.The Potentials and Caveats of Mesenchymal Stromal Cell-Based Therapies in the Preterm Infant.

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P2860

Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.

http://www.wikidata.org/entity/Q41824496

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2012年の論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.

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type

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Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.

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prefLabel

Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.

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Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.

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Cristina M Alvira

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David N Cornfield

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Eloa S Adams

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Shu-Chen Lyu

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Yanli Hou

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Immunity, Inflammation, and Cancer

Integrating cell-signalling pathways with NF-kappaB and IKK function

NF-kappa B RelA-deficient lymphocytes: normal development of T cells and B cells, impaired production of IgA and IgG1 and reduced proliferative responses

Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-kappa B

Vascular endothelial growth factor gene therapy increases survival, promotes lung angiogenesis, and prevents alveolar damage in hyperoxia-induced lung injury: evidence that angiogenesis participates in alveolarization

Shared principles in NF-kappaB signaling

Ineffectiveness of histone deacetylase inhibitors to induce apoptosis involves the transcriptional activation of NF-kappa B through the Akt pathway.

IKKβ regulates essential functions of the vascular endothelium through kinase-dependent and -independent pathways

NF-kappa B mediates up-regulation of CFTR gene expression in Calu-3 cells by interleukin-1beta.

Phase I trial of the proteasome inhibitor PS-341 in patients with refractory hematologic malignancies.

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