A group led by Dr. Sem Phan at the University of Michigan, Ann Arbor identified Notch1 as a mediator of lung fibrosis.
They present their data in the May 2009 issue of The American Journal of Pathology.
Scar tissue, or fibrosis, can accumulate in the lungs, restricting the flow of oxygen and leading to end-stage lung disease, respiratory failure, and eventually death. An increase in the number of a special type of cells, myofibroblasts, strongly contributes to lung fibrosis.
FIZZ1, a protein found in the lungs, increases the number of myofibroblasts in the lungs. Liu et al hypothesized that Notch1, which regulates cell fate in numerous cell types, plays a role in FIZZ1-mediated myofibroblast differentiation. They found that Notch1 led to an increase of myofibroblasts in the lungs, and that mice that lacked Notch1 had decreased responses to FIZZ1 and lower levels of lung fibrosis.
Taken together, these data suggest that "Notch1 signaling in response to FIZZ1 may play a significant role in myofibroblast differentiation during lung fibrosis." Therefore, Notch1 may provide a novel target for treatment of scar tissue in the lungs.
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