期刊
CELL BIOCHEMISTRY AND BIOPHYSICS
卷 43, 期 1, 页码 131-148出版社
HUMANA PRESS INC
DOI: 10.1385/CBB:43:1:131
关键词
asthma; chronic obstructive pulmonary disease; lymphangioleiomyomatosis; inflammation; cytokine; transforming growth factor-beta; emphysema; smooth muscle; tumor
资金
- NHLBI NIH HHS [HL5639] Funding Source: Medline
The transforming growth factor (TGF) superfamily encompasses about 30 members in mammals. The effect of TGF-beta subfamily members is exerted and regulated via selective pathways of synthesis and signaling that involve activation of latent TGF-beta, specific and high-affinity binding to cell membrane serine/threonine kinase receptors, activation of intracellular cascades that include Smad molecules and mitogen-activated protein kinases, and regulated termination of the effect by diverse mechanisms including protein degradation and transcriptional activation. Several comprehensive reviews on TGF-beta biology in general and on the role of this cytokine in other diseases have been published recently. In recent years an unexpected role of TGF-beta on lung homeostasis has been revealed. Here, we discuss the contribution of TGF-beta to the pathogenesis of asthma and chronic obstructive pulmonary disease, two common illnesses of the lung, as well as of lymphangioleiomyomatosis, a rare disease in women. The information we collate and integrate places TGF-beta at a pivotal point within complex networks that control lung physiology as well as the physiopathology of these lung diseases.
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