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肺动脉高压发病机制中瓦博格效应与炎性细胞因子的分子靶点

Molecular targets of the Warburg effect and inflammatory cytokines in the pathogenesis of pulmonary artery hypertension.

作者信息

Liu Na, Parry Stephanie, Xiao Yunbin, Zhou Shenghua, Liu Qiming

机构信息

Department of Cardiology and Cardiac Catheterization Lab, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.

University of Nebraska Medical Center, United States.

出版信息

Clin Chim Acta. 2017 Mar;466:98-104. doi: 10.1016/j.cca.2017.01.015. Epub 2017 Jan 14.

Abstract

Pulmonary arterial hypertension (PAH) is a progressive vascular disease characterized by increased pulmonary arterial pressure and vasoconstriction and structural remolding of pulmonary arterioles. Recent clinical and experimental studies have discovered the relationship between metabolic alterations and the pathogenesis of PAH. The primary metabolic alteration, previously demonstrated in various cancers, is a gradual change in energy generated from complete aerobic cellular respiration to from solely "aerobic glycolysis," termed the "Warburg effect." Understanding the Warburg effect of metabolic dysregulation and its interaction with inflammatory mechanisms in the pathogenesis of PAH has provided a valuable explanation of this disease and has guided formulation of new clinical treatments at the molecular level.

摘要

肺动脉高压(PAH)是一种进行性血管疾病,其特征是肺动脉压力升高、肺小动脉血管收缩和结构重塑。最近的临床和实验研究发现了代谢改变与PAH发病机制之间的关系。先前在各种癌症中得到证实的主要代谢改变,是能量从完全有氧细胞呼吸逐渐转变为仅来自“有氧糖酵解”,即所谓的“瓦伯格效应”。了解代谢失调的瓦伯格效应及其在PAH发病机制中与炎症机制的相互作用,为这种疾病提供了有价值的解释,并在分子水平上指导了新的临床治疗方案的制定。

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