| pubmed-article:18094078 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18094078 | lifeskim:mentions | umls-concept:C1267092 | lld:lifeskim |
| pubmed-article:18094078 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
| pubmed-article:18094078 | lifeskim:mentions | umls-concept:C0439659 | lld:lifeskim |
| pubmed-article:18094078 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18094078 | pubmed:dateCreated | 2007-12-20 | lld:pubmed |
| pubmed-article:18094078 | pubmed:abstractText | Airway smooth muscle (SM) develops from local mesenchymal cells located around the tips of growing epithelial buds. These cells gradually displace from distal to proximal position alongside the bronchial tree, elongate, and begin to synthesize SM-specific proteins. Mechanical tension (either generated by cell spreading/elongation or stretch), as well as epithelial paracrine factors, regulates the process of bronchial myogenesis. The specific roles of many of these paracrine factors during normal lung development are currently unknown. It is also unknown how and if mechanical and paracrine signals integrate into a common myogenic pathway. Furthermore, as with vascular SM and other types of visceral SM, we are just beginning to elucidate the intracellular signaling pathways and the genetic program that controls lung myogenesis. Here we present what we have learned so far about the embryogenesis of bronchial muscle. | lld:pubmed |
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| pubmed-article:18094078 | pubmed:language | eng | lld:pubmed |
