期刊
PULMONARY PHARMACOLOGY & THERAPEUTICS
卷 26, 期 1, 页码 50-63出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pupt.2012.07.006
关键词
Asthma; Chronic obstructive pulmonary disease; WNT/beta-catenin signaling; PI3K signaling; Calcium; Autophagy; S100 proteins; HMGB1
资金
- Parker B Francis Fellowship in Respiratory disease
- Manitoba Health Research Council (MHRC) postdoctoral fellowship
- Netherlands Asthma Foundation [3.2.07.023]
- University of Groningen
The airway smooth muscle (ASM) plays an important role in the pathophysiology of asthma and chronic obstructive pulmonary disease (COPD). ASM cells express a wide range of receptors involved in contraction, growth, matrix protein production and the secretion of cytokines and chemokines. Transforming growth factor beta (TGF-beta) is one of the major players in determining the structural and functional abnormalities of the ASM in asthma and COPD. It is increasingly evident that TGF-beta functions as a master switch, controlling a network of intracellular and autocrine signaling loops that effect ASM phenotype and function. In this review, the various elements that participate in non-canonical TGF-beta signaling, including MAPK, PI3K, WNT/beta-catenin, and Ca2+, are discussed, focusing on their effect on ASM phenotype and function. In addition, new aspects of ASM biology and their possible association with non-canonical TGF-beta signaling will be discussed. (C) 2012 Elsevier Ltd. All rights reserved.
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