期刊
ANNUAL REVIEW OF PHYSIOLOGY, VOL 73
卷 73, 期 -, 页码 413-435出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-012110-142225
关键词
TGF beta 1; integrin; fibrogenesis; beta-catenin
类别
资金
- NHLBI NIH HHS [HL44712, R01 HL044712] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL044712] Funding Source: NIH RePORTER
Lung epithelial cells have emerged as a frequent target of injury, a driver of normal repair, and a key element in the pathobiology of fibrotic lung diseases. An important aspect of epithelial cells is their capacity to respond to microenvironmental cues by undergoing epithelial-mesenchymal transition (EMT). EMT is not simply widespread conversion of epithelial cells to fibroblasts but a graded response whereby epithelial cells reversibly acquire mesenchymal features and enhanced capacity for mesenchymal cross-talk. Recent studies elucidate distinct integrin-sensing systems that coordinate activity of TGF beta 1, a critical signaling element regulating EMT, with the presence of proinflammatory signals and cell injury. Repeated injury superimposes persistent inflammation and hypoxia onto these highly regulated repair pathways, potentially overwhelming orderly repair and creating sustained fibrogenesis. Understanding specific signaling mechanisms driving the mesenchymal response to TGF beta 1 may reveal therapeutics to attenuate fibrogenesis yet preserve the important homeostatic functions of TGF beta 1.
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