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Carlyne D. Cool

Researcher at University of Colorado Denver

Publications -  181
Citations -  14771

Carlyne D. Cool is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Pulmonary hypertension & Lung. The author has an hindex of 62, co-authored 164 publications receiving 13497 citations. Previous affiliations of Carlyne D. Cool include University of Colorado Boulder & University of California, Davis.

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Prostacyclin Synthase Expression Is Decreased in Lungs from Patients with Severe Pulmonary Hypertension

TL;DR: It is concluded that the different sizes of the pulmonary arteries express PGI2-S differently and that the loss of expression of PGI1 synthase represents one of the phenotypic alterations present in the pulmonary endothelial cells in severe PH.
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Endothelial cell death and decreased expression of vascular endothelial growth factor and vascular endothelial growth factor receptor 2 in emphysema.

TL;DR: It is proposed that epithelial and endothelial alveolar septal death due to a decrease of endothelial cell maintenance factors may be part of the pathogenesis of emphysema.
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Expression of angiogenesis‐related molecules in plexiform lesions in severe pulmonary hypertension: evidence for a process of disordered angiogenesis

TL;DR: It is postulated that in lungs with SPH, endothelial cells in plexiform lesions express genes encoding for proteins involved in angiogenesis, in particular, vascular endothelial growth factor (VEGF) and those involved in VEGF receptor‐2 (VEGFR‐2) signalling.
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Modern age pathology of pulmonary arterial hypertension.

TL;DR: The results indicate that multiple features of pulmonary vascular remodeling are present in patients treated with modern PAH therapies, and perivascular inflammation may have an important role in the processes ofascular remodeling, all of which may ultimately lead to increased pulmonary artery pressure.
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Formation of plexiform lesions in experimental severe pulmonary arterial hypertension

TL;DR: Severe, sustained pulmonary hypertension in a very late stage of the Sugen 5416/hypoxia/normoxia-exposed rat is accompanied by the formation of lesions that are indistinguishable from the pulmonary arteriopathy of human pulmonary arterial hypertension.