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Autor:
Andrea L. Frump, Mona Selej, Bakhtiyor Yakubov, Marjorie Albrecht, Irina Petrache, Jordan A. Wood, Tim Lahm
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 59:114-126
17β-Estradiol (E2) attenuates hypoxia-induced pulmonary hypertension (HPH) through estrogen receptor (ER)-dependent effects, including inhibition of hypoxia-induced endothelial cell proliferation; however, the mechanisms responsible for this remain
Autor:
Teja Gregorc, Craig K. Docherty, Afshan Dean, Margaret R. MacLean, Katie Y. Harvey, Margaret Nilsen, Nicholas W. Morrell
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 58:320-330
Rationale: Rats dosed with the vascular endothelial growth factor (VEGF) inhibitor Sugen 5416 (Su), placed in hypoxia then restored to normoxia has become a widely used model of pulmonary arterial hypertension (PAH). The mechanism by which Su exaccer
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 55:368-376
High serotonin levels during pregnancy affect central nervous system development. Whether a commonly used antidepressant such as fluoxetine (a selective serotonin reuptake inhibitor) taken during pregnancy may adversely affect respiratory control in
Autor:
Fayong Luo, Lavannya M. Pandit, Javier Amione-Guerra, Tingting Weng, Harry Karmouty-Quintana, Michael R. Blackburn, Kelly A. Volcik, Brian A. Bruckner, Matthias Loebe, Kemly Philip, Ernestina Melicoff, Holger K. Eltzschig, R.R. Bunge, Jonathan Davies, Luis J. Garcia-Morales, Ning Yuan Chen
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 54:574-583
Group III pulmonary hypertension (PH) is a highly prevalent and deadly lung disorder with limited treatment options other than transplantation. Group III PH affects patients with ongoing chronic lung injury, such as idiopathic pulmonary fibrosis (IPF
Autor:
Jung Whan Kim, Vladimir Shulaev, Meng Hsiung Hsieh, Norihiko Takeda, Shanta Dhar, Pankaj K. Singh, Jung-Mo Ahn, Inkyu Lee, Heather N. Hayenga, Hyunsung Choi, David B. Shackelford, Justin Goodwin, Michael L. Neugent
Hypoxia has long been implicated in the pathogenesis of fibrotic diseases. Aberrantly activated myofibroblasts are the primary pathological driver of fibrotic progression, yet how various microenvironmental influences, such as hypoxia, contribute to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5c9e0e175313b74a54329ac13eb126d7
https://europepmc.org/articles/PMC5805994/
https://europepmc.org/articles/PMC5805994/
Autor:
Wei Luo, Shan Huang, Pingsheng Wu, Wei Li, Shao-Xi Cai, Xu Li, Chang-Hui Yu, Ting Li, Ying Meng
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 50:723-736
Accumulating evidence has demonstrated that up-regulation of the angiotensin (Ang)-converting enzyme (ACE)/AngII/AngII type 1 receptor (AT1R) axis aggravates pulmonary fibrosis. The recently discovered ACE2/Ang-(1-7)/Mas axis, which counteracts the a
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 50:559-570
The diagnosis of chronic obstructive pulmonary disease (COPD) confers a 2-fold increased lung cancer risk even after adjusting for cigarette smoking, suggesting that common pathways are operative in both diseases. Although the role of the tyrosine ki
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 50:74-86
Despite improvements in survival with disease-targeted therapies, the majority of patients with pulmonary arterial hypertension (PAH) have persistent exercise intolerance that results from impaired cardiac function and skeletal muscle dysfunction. Ou
Autor:
Zoya V. Niatsetskaya, Irina Utkina-Sosunova, Sergey A. Sosunov, Veniamin Ratner, Vadim S. Ten
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 49:943-950
Hyperoxia inhibits pulmonary bioenergetics, causing delayed alveolarization in mice. We hypothesized that mechanical ventilation (MV) also causes a failure of bioenergetics to support alveolarization. To test this hypothesis, neonatal mice were venti
Autor:
Henry T. Akinbi, John E. Baatz, Joseph A. Kitzmiller, Yan Xu, Kristen Page, Thomas R. Korfhagen, Stephan W. Glasser, Teah L. Ruetschilling, Melissa D. Maxfield, Erik L. Bao
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 49:845-854
Pulmonary surfactant protein-C (SP-C) gene-targeted mice (Sftpc(-/-)) develop progressive lung inflammation and remodeling. We hypothesized that SP-C deficiency reduces the ability to suppress repetitive inflammatory injury. Sftpc(+/+) and Sftpc(-/-)