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Cellular and molecular pathobiology of pulmonary arterial hypertension.
Pulmonary arterial hypertension (PAH) has a multifactorial pathobiology. Vasoconstriction, remodeling of the pulmonary vessel wall, and thrombosis contribute to increased pulmonary vascularExpand
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Molecular pathogenesis of pulmonary arterial hypertension.
Recent investigations have suggested that it might be possible to reverse the pathology of pulmonary arterial hypertension (PAH), a disorder that can be rapidly progressive and fatal despite currentExpand
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Subversion of Cellular Autophagosomal Machinery by RNA Viruses
Infection of human cells with poliovirus induces the proliferation of double-membraned cytoplasmic vesicles whose surfaces are used as the sites of viral RNA replication and whose origin is unknown.Expand
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Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension.
This review summarizes an expanding body of knowledge indicating that failure to resolve inflammation and altered immune processes underlie the development of pulmonary arterial hypertension. TheExpand
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Rat pulmonary circulation after chronic hypoxia: hemodynamic and structural features.
In 55 Sprague-Dawley rats (mean wt, 277 +/- 6.2 g) exposed to hypobaric hypoxia (air at 380 mmHg), and 23 weight-matched controls kept in room air, pulmonary and systemic artery pressures wereExpand
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Interdependent Serotonin Transporter and Receptor Pathways Regulate S100A4/Mts1, a Gene Associated With Pulmonary Vascular Disease
Heightened expression of the S100 calcium–binding protein, S100A4/Mts1, is observed in pulmonary vascular disease. Loss of serotonin (5-hydroxytryptamine [5-HT]) receptors or of the serotoninExpand
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FK506 activates BMPR2, rescues endothelial dysfunction, and reverses pulmonary hypertension.
Dysfunctional bone morphogenetic protein receptor-2 (BMPR2) signaling is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). We used a transcriptional high-throughput luciferaseExpand
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Pulmonary arterial hypertension is linked to insulin resistance and reversed by peroxisome proliferator-activated receptor-gamma activation.
BACKGROUND Patients with pulmonary arterial hypertension (PAH) have reduced expression of apolipoprotein E (apoE) and peroxisome proliferator-activated receptor-gamma in lung tissues, and deficiencyExpand
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Elastase and matrix metalloproteinase inhibitors induce regression, and tenascin-C antisense prevents progression, of vascular disease.
Increased expression of the glycoprotein tenascin-C (TN) is associated with progression of clinical and experimental pulmonary hypertension. In cultured smooth muscle cells (SMCs) TN is induced byExpand
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Pulmonary arterial remodeling induced by a Th2 immune response
Daley et al. 2008. J. Exp. Med. doi:10.1084/jem.20071008[OpenUrl][1][Abstract/FREE Full Text][2] [1]:Expand
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