کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5955001 | 1173324 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
New Molecular Targets of Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension
ترجمه فارسی عنوان
اهداف مولکولی جدید تجدید ساختار عروقی ریوی در فشار خون بالا ریه
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کلمات کلیدی
PGI25-HTRegulatory T lymphocyteMMPmPAPTregANGIIMCPPAHSMCTGFBMPRIIECMFGFAngiotensin II - آنژیوتانسین دوendothelin - اندوتلینtransforming growth factor - تبدیل فاکتور رشدSerotonin - سروتونینSmooth muscle cell - سلول عضلانی صافEndothelial cell - سلول های اندوتلیالMIF - شهرMigration inhibitory factor - عامل مهارکننده مهاجرتfibroblast growth factor - فاکتور رشد فیبروبلاستPulmonary arterial hypertension - فشار خون شریانی ریویmean pulmonary arterial pressure - فشار متوسط شریان ریویExtracellular matrix - ماتریکس خارج سلولیmatrix metalloproteinase - ماتریکس متالوپروتئینازMicroRNA - میکرو RNA MiRNA - میکروRNA، ریزآرانای، miRNANitric oxide - نیتریک اکسیدPulmonary hypertension - پرفشاری خون ریویmonocyte chemoattractant protein - پروتئین شیمیایی monocyte chemoattractantprostacyclin - پروستاسیکلین
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
چکیده انگلیسی
Pulmonary arterial hypertension (PAH) is a disorder in which mechanical obstruction of the pulmonary vascular bed is largely responsible for the rise in mean pulmonary arterial pressure, resulting in a progressive functional decline despite current available therapeutic options. The fundamental pathogenetic mechanisms underlying this disorder include pulmonary vasoconstriction, in situ thrombosis, medial hypertrophy, and intimal proliferation, leading to occlusion of the small to mid-sized pulmonary arterioles and the formation of plexiform lesions. Several predisposing or promoting mechanisms that contribute to excessive pulmonary vascular remodeling in PAH have emerged, such as altered crosstalk between cells within the vascular wall, sustained inflammation and dysimmunity, inhibition of cell death, and excessive activation of signaling pathways, in addition to the impact of systemic hormones, local growth factors, cytokines, transcription factors, and germline mutations. Although the spectrum of therapeutic options for PAH has expanded in the last 20 years, available therapies remain essentially palliative. However, over the past decade, a better understanding of new key regulators of this irreversible pulmonary vascular remodeling has been obtained. This review examines the state-of-the-art potential new targets for innovative research in PAH, focusing on (1) the crosstalk between cells within the pulmonary vascular wall, with particular attention to the role played by dysfunctional endothelial cells; (2) aberrant inflammatory and immune responses; (3) the abnormal extracellular matrix function; and (4) altered BMPRII/KCNK3 signaling systems. A better understanding of novel pathways and therapeutic targets will help in the designing of new and more effective approaches for PAH treatment.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chest - Volume 147, Issue 2, February 2015, Pages 529-537
Journal: Chest - Volume 147, Issue 2, February 2015, Pages 529-537
نویسندگان
Christophe PhD, Ly PhD, Barbara PhD, Nicolas PhD, Alice MD, PhD, David MD, PhD, Marc MD, PhD,