mTOR is required for pulmonary arterial vascular smooth muscle cell proliferation under chronic hypoxia.
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The critical role of Akt in cardiovascular functionPulmonary hypertension in lymphangioleiomyomatosis: prevalence, severity and the role of carbon monoxide diffusion capacity as a screening methodBaicalin inhibits hypoxia-induced pulmonary artery smooth muscle cell proliferation via the AKT/HIF-1α/p27-associated pathwaymTORC2 is required for proliferation and survival of TSC2-null cells.A cell permeable peptide targeting the intracellular loop 2 of endothelin B receptor reduces pulmonary hypertension in a hypoxic rat modelDeficiency of Akt1, but not Akt2, attenuates the development of pulmonary hypertension.Hyperplastic Growth of Pulmonary Artery Smooth Muscle Cells from Subjects with Pulmonary Arterial Hypertension Is Activated through JNK and p38 MAPK.A Critical Role of the mTOR/eIF2α Pathway in Hypoxia-Induced Pulmonary Hypertension.Rapamycin decreases airway remodeling and hyperreactivity in a transgenic model of noninflammatory lung disease.PDGF enhances store-operated Ca2+ entry by upregulating STIM1/Orai1 via activation of Akt/mTOR in human pulmonary arterial smooth muscle cells.Metformin attenuates hyperoxia-induced lung injury in neonatal rats by reducing the inflammatory responseDifferential effects of formoterol on thrombin- and PDGF-induced proliferation of human pulmonary arterial vascular smooth muscle cells.A novel nontoxic inhibitor of the activation of NADPH oxidase reduces reactive oxygen species production in mouse lung.mTOR and vascular remodeling in lung diseases: current challenges and therapeutic prospects.Rapamycin reverses pulmonary artery smooth muscle cell proliferation in pulmonary hypertensionUp-regulation of the mammalian target of rapamycin complex 1 subunit Raptor by aldosterone induces abnormal pulmonary artery smooth muscle cell survival patterns to promote pulmonary arterial hypertensionCalpain-2 activates Akt via TGF-β1-mTORC2 pathway in pulmonary artery smooth muscle cellsAdenosine monophosphate-activated protein kinase is required for pulmonary artery smooth muscle cell survival and the development of hypoxic pulmonary hypertensionGerminal centre hypoxia and regulation of antibody qualities by a hypoxia response system.Mammalian target of rapamycin complex 2 (mTORC2) coordinates pulmonary artery smooth muscle cell metabolism, proliferation, and survival in pulmonary arterial hypertension.Emerging role of selective autophagy in human diseases.Autophagy in lung disease pathogenesis and therapeutics.Mesoglycan attenuates VSMC proliferation through activation of AMP-activated protein kinase and mTOR.Pharmacological Inhibition of mTOR Kinase Reverses Right Ventricle Remodeling and Improves Right Ventricle Structure and Function in Rats.Biocompatible reactive oxygen species (ROS)-responsive nanoparticles as superior drug delivery vehicles.Pulmonary Hypertension and Cancer: Etiology, Diagnosis, and Management.HIPPO-Integrin-linked Kinase Cross-Talk Controls Self-Sustaining Proliferation and Survival in Pulmonary Hypertension.Regulation of autophagy and its associated cell death by "sphingolipid rheostat": reciprocal role of ceramide and sphingosine 1-phosphate in the mammalian target of rapamycin pathway.mTOR-Notch3 signaling mediates pulmonary hypertension in hypoxia-exposed neonatal rats independent of changes in autophagy.TOR signaling couples oxygen sensing to lifespan in C. elegans.Melatonin attenuates hypoxic pulmonary hypertension by inhibiting the inflammation and the proliferation of pulmonary arterial smooth muscle cells.Suppression of endothelial PGC-1α is associated with hypoxia-induced endothelial dysfunction and provides a new therapeutic target in pulmonary arterial hypertension.Salidroside attenuates hypoxia-induced pulmonary arterial smooth muscle cell proliferation and apoptosis resistance by upregulating autophagy through the AMPK-mTOR-ULK1 pathway.Emerging Therapeutics in Pulmonary Hypertension.Endothelial cell-related autophagic pathways in Sugen/hypoxia-exposed pulmonary arterial hypertensive rats.Translational Advances in the Field of Pulmonary Hypertension. From Cancer Biology to New Pulmonary Arterial Hypertension Therapeutics. Targeting Cell Growth and Proliferation Signaling Hubs.mTOR: A Key to Both Pulmonary Vessel Remodeling and Right Ventricular Function in Pulmonary Arterial Hypertension?mTORC1 is involved in hypoxia-induced pulmonary hypertension through the activation of Notch3.Selective Tuberous Sclerosis Complex 1 Gene Deletion in Smooth Muscle Activates Mammalian Target of Rapamycin Signaling and Induces Pulmonary Hypertension.
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mTOR is required for pulmonary arterial vascular smooth muscle cell proliferation under chronic hypoxia.
description
2011 nî lūn-bûn
@nan
2011 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի մարտին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
mTOR is required for pulmonary ...... eration under chronic hypoxia.
@ast
mTOR is required for pulmonary ...... eration under chronic hypoxia.
@en
type
label
mTOR is required for pulmonary ...... eration under chronic hypoxia.
@ast
mTOR is required for pulmonary ...... eration under chronic hypoxia.
@en
prefLabel
mTOR is required for pulmonary ...... eration under chronic hypoxia.
@ast
mTOR is required for pulmonary ...... eration under chronic hypoxia.
@en
P2093
P2860
P356
P1433
P1476
mTOR is required for pulmonary ...... eration under chronic hypoxia.
@en
P2093
Dmitry A Goncharov
Elena A Goncharova
Gregory Cesarone
Irene Khavin
Jennifer Snow
Kaori Ihida-Stansbury
Peter L Jones
Poay N Lim
Sigrid C Veasey
Vera P Krymskaya
P2860
P304
P356
10.1096/FJ.10-175018
P407
P577
2011-03-02T00:00:00Z