EMT and interstitial lung disease: a mysterious relationship
H Kage, Z Borok - Current opinion in pulmonary medicine, 2012 - journals.lww.com
H Kage, Z Borok
Current opinion in pulmonary medicine, 2012•journals.lww.comAdvances have been made in elucidating causes and mechanisms of EMT, potentially
leading to new treatment options, although contributions of EMT to lung fibrosis in vivo
remain controversial. In addition to EMT providing a direct source of (myo) fibroblasts,
expression of mesenchymal markers may reflect epithelial injury, in which case inhibition of
EMT might be deleterious. EMT-derived cells may also contribute to aberrant epithelial–
mesenchymal crosstalk that promotes fibrogenesis.
leading to new treatment options, although contributions of EMT to lung fibrosis in vivo
remain controversial. In addition to EMT providing a direct source of (myo) fibroblasts,
expression of mesenchymal markers may reflect epithelial injury, in which case inhibition of
EMT might be deleterious. EMT-derived cells may also contribute to aberrant epithelial–
mesenchymal crosstalk that promotes fibrogenesis.
Summary
Advances have been made in elucidating causes and mechanisms of EMT, potentially leading to new treatment options, although contributions of EMT to lung fibrosis in vivo remain controversial. In addition to EMT providing a direct source of (myo) fibroblasts, expression of mesenchymal markers may reflect epithelial injury, in which case inhibition of EMT might be deleterious. EMT-derived cells may also contribute to aberrant epithelial–mesenchymal crosstalk that promotes fibrogenesis.
Lippincott Williams & Wilkins