دورية أكاديمية
أعرض في EDS

Pathogenic Role of mTORC1 and mTORC2 in Pulmonary Hypertension.

التفاصيل البيبلوغرافية
العنوان: Pathogenic Role of mTORC1 and mTORC2 in Pulmonary Hypertension.
المؤلفون: Tang H; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China., Wu K; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China., Wang J; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China., Vinjamuri S; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Gu Y; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Song S; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Wang Z; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China., Zhang Q; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.; Department of Physiology, The University of Arizona College of Medicine, Tucson, Arizona., Balistrieri A; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Ayon RJ; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Rischard F; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Vanderpool R; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Chen J; Department of Pediatrics, University of Illinois College of Medicine, Chicago, Illinois., Zhou G; State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.; Department of Pediatrics, University of Illinois College of Medicine, Chicago, Illinois., Desai AA; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; Division of Cardiology, Department of Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Black SM; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; Department of Physiology, The University of Arizona College of Medicine, Tucson, Arizona., Garcia JGN; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; Department of Physiology, The University of Arizona College of Medicine, Tucson, Arizona.; Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, The University of Arizona College of Medicine, Tucson, Arizona., Yuan JX; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.; Department of Physiology, The University of Arizona College of Medicine, Tucson, Arizona., Makino A; Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.; Department of Physiology, The University of Arizona College of Medicine, Tucson, Arizona.
المصدر: JACC. Basic to translational science [JACC Basic Transl Sci] 2018 Dec 31; Vol. 3 (6), pp. 744-762. Date of Electronic Publication: 2018 Dec 31 (Print Publication: 2018).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier on behalf of the American College of Cardiology Foundation Country of Publication: United States NLM ID: 101677259 Publication Model: eCollection Cited Medium: Internet ISSN: 2452-302X (Electronic) Linking ISSN: 2452302X NLM ISO Abbreviation: JACC Basic Transl Sci Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [New York] : Elsevier on behalf of the American College of Cardiology Foundation, [2016]-
مستخلص: Concentric lung vascular wall thickening due to enhanced proliferation of pulmonary arterial smooth muscle cells is an important pathological cause for the elevated pulmonary vascular resistance reported in patients with pulmonary arterial hypertension. We identified a differential role of mammalian target of rapamycin (mTOR) complex 1 and complex 2, two functionally distinct mTOR complexes, in the development of pulmonary hypertension (PH). Inhibition of mTOR complex 1 attenuated the development of PH; however, inhibition of mTOR complex 2 caused spontaneous PH, potentially due to up-regulation of platelet-derived growth factor receptors in pulmonary arterial smooth muscle cells, and compromised the therapeutic effect of the mTOR inhibitors on PH. In addition, we describe a promising therapeutic strategy using combination treatment with the mTOR inhibitors and the platelet-derived growth factor receptor inhibitors on PH and right ventricular hypertrophy. The data from this study provide an important mechanism-based perspective for developing novel therapies for patients with pulmonary arterial hypertension and right heart failure.
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معلومات مُعتمدة: P01 HL134610 United States HL NHLBI NIH HHS; R01 HL137282 United States HL NHLBI NIH HHS; R01 HL142214 United States HL NHLBI NIH HHS; T32 HD049303 United States HD NICHD NIH HHS; R01 HL136603 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: EC, endothelial cell; FOXO3a, Forkhead box O3a; GPCR, G protein-coupled receptor; HPH, hypoxia-induced pulmonary hypertension; PA, pulmonary artery; PAEC, pulmonary arterial endothelial cell; PAH, pulmonary arterial hypertension; PASMC, pulmonary arterial smooth muscle cell; PDGF, platelet-derived growth factor; PDGFR, platelet-derived growth factor receptor; PH, pulmonary hypertension; PI3K, phosphoinositide 3-kinase; PTEN, phosphatase and tensin homolog; PVR, pulmonary vascular resistance; RVH, right ventricular hypertrophy; RVSP, right ventricular systolic pressure; Raptor; Raptor, regulatory associated protein of mammalian target of rapamycin; Rictor; Rictor, rapamycin insensitive companion of mammalian target of rapamycin; SM, smooth muscle; TKR, tyrosine kinase receptor; WT, wild-type; mTOR; mTORC1, mammalian target of rapamycin complex 1; mTORC2, mammalian target of rapamycin complex 2; pAKT, phosphorylated AKT; pulmonary hypertension; right ventricle
تواريخ الأحداث: Date Created: 20190110 Latest Revision: 20210720
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC6314964
DOI: 10.1016/j.jacbts.2018.08.009
PMID: 30623134
قاعدة البيانات: MEDLINE
الوصف
تدمد:2452-302X
DOI:10.1016/j.jacbts.2018.08.009