pulmonary fibrosis/hypoxia

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Diverse echocardiographic changes in the course of hypoxia due to acute exacerbation of idiopathic pulmonary fibrosis

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Idiopathic pulmonary fibrosis (IPF) is a progressive parenchymal disease. Pulmonary hypertension (PH) is a potentially lethal complication in the course of IPF. In almost all cases of IPF-PH there is gradual deterioration, but patients can also decline suddenly due to hypoxia. This case report

Role of impaired peritubular capillary and hypoxia in progressive interstitial fibrosis after 56 subtotal nephrectomy of rats.

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OBJECTIVE To investigate the potential role of peritubular capillary (PTC) loss and subsequent hypoxia as a pathogenic factor in interstitial fibrosis after renal ablation in rats. METHODS PTC loss and tubulointerstitial hypoxia in remnant kidney rats (SNTx group), sham-operated rats (sham group)

Chronic intermittent hypoxia worsens bleomycin-induced lung fibrosis in rats.

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Obstructive sleep apnea (OSA) has been linked to increased mortality in pulmonary fibrosis. Its key feature, chronic intermittent hypoxia (CIH), can lead to oxidative stress and inflammation, known to lead to fibrotic pathology in other organs. We tested the effects of CIH in an animal model of

Hypoxia-induced deoxycytidine kinase contributes to epithelial proliferation in pulmonary fibrosis.

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BACKGROUND Idiopathic pulmonary fibrosis (IPF) is a deadly lung disease with few therapeutic options. Apoptosis of alveolar epithelial cells, followed by abnormal tissue repair characterized by hyperplastic epithelial cell formation, is a pathogenic process that contributes to the progression of

Hypoxia-Induced Epithelial-Mesenchymal Transition Is Involved in Bleomycin-Induced Lung Fibrosis.

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Pulmonary fibrosis is a severe disease that contributes to the morbidity and mortality of a number of lung diseases. However, the molecular and cellular mechanisms leading to lung fibrosis are poorly understood. This study investigated the roles of epithelial-mesenchymal transition (EMT) and the

The Effects of Chronic Intermittent Hypoxia in Bleomycin-induced lung injury on Pulmonary Fibrosis via Regulating the NF-κB/Nrf2 Signaling Pathway

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Background: Obstructive sleep apnea (OSA) is associated with pulmonary fibrosis. Chronic intermittent hypoxia (CIH) is considered to be a surrogate of OSA. However, its exact role in pulmonary fibrosis remains uncertain. Therefore, we

Increased hemoglobin-oxygen affinity ameliorates bleomycin-induced hypoxemia and pulmonary fibrosis.

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Although exertional dyspnea and worsening hypoxia are hallmark clinical features of idiopathic pulmonary fibrosis (IPF), no drug currently available could treat them. GBT1118 is a novel orally bioavailable small molecule that binds to hemoglobin and produces a concentration-dependent left shift of

Improvement in pulmonary hypertension and hypoxemia during nitric oxide inhalation in a patient with end-stage pulmonary fibrosis.

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A patient with severe interstitial pulmonary fibrosis, hypoxemia, pulmonary hypertension, and cor pulmonale was given inhaled nitric oxide (NO) followed by intravenous PGE1 to assess the reversibility of pulmonary hypertension. During NO inhalation, there was marked reduction in pulmonary vascular

Inflammatory response mechanisms exacerbating hypoxemia in coexistent pulmonary fibrosis and sleep apnea.

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Mediators of inflammation, oxidative stress, and chemoattractants drive the hypoxemic mechanisms that accompany pulmonary fibrosis. Patients with idiopathic pulmonary fibrosis commonly have obstructive sleep apnea, which potentiates the hypoxic stimuli for oxidative stress, culminating in systemic

24-Hour Hypoxia and Pulmonary Hypertension in Patients with Idiopathic Pulmonary Fibrosis.

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BACKGROUND The quantification of hypoxia based on resting partial pressure of arterial oxygen (PaO2) may underestimate hypoxia related to activities of daily living or sleep and thus not accurately reflect pulmonary hypertension (PH). The aim of the present study was to investigate the association

Suboptimal erythropoietic response to hypoxemia in idiopathic pulmonary fibrosis.

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OBJECTIVE Idiopathic pulmonary fibrosis (IPF) is a chronic inflammatory process characterized by severe derangement of gas exchange in the advanced stages of disease. However, erythrocytosis is infrequent in IPF. The aim of this study was to investigate the potential relation between the blunted

Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase.

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Pulmonary fibrosis (PF) is one of the most prevalent causes of death following paraquat (PQ) poisoning. As demonstrated in previous studies by the present authors, epithelial-to-mesenchymal transition (EMT) is associated with PQ-induced PF. In addition, hypoxia-inducible factor-1α (HIF-1α) and lysyl

The Akt inhibitor, triciribine, ameliorates chronic hypoxia-induced vascular pruning and TGFβ-induced pulmonary fibrosis.

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OBJECTIVE Interstitial lung disease accounts for a group of chronic and progressive disorders associated with severe pulmonary vascular remodelling, peripheral vascular rarefaction and fibrosis, thus limiting lung function. We have previously shown that Akt is necessary for myofibroblast

Hypoxia-inducible factor-1α mediates TGF-β-induced PAI-1 production in alveolar macrophages in pulmonary fibrosis.

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Hypoxia-inducible factor-1α (HIF-1α), a transcription factor that functions as a master regulator of oxygen homeostasis, has been implicated in fibrinogenesis. Here, we explore the role of HIF-1α in transforming growth factor-β (TGF-β) signaling by examining the effects of TGF-β(1) on the expression

Comparative expression profiling in pulmonary fibrosis suggests a role of hypoxia-inducible factor-1alpha in disease pathogenesis.

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BACKGROUND Despite intense research efforts, the etiology and pathogenesis of idiopathic pulmonary fibrosis remain poorly understood. OBJECTIVE To discover novel genes and/or cellular pathways involved in the pathogenesis of the disease. METHODS We performed expression profiling of disease

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