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WISP-1 is upregulated in human patients with idiopathic pulmonary fibrosis and in a mouse model of bleomycin-induced lung fibrosis. [30] Orotracheal application of CCN4 neutralizing antibodies to the lung ameliorates bleomycin-induced lung fibrosis, [30] raising the possibility that CCN4 might be a potential target for anti-fibrotic therapy. [5]
Precision-cut Lung Slices (PCLS) have proven effective in studying the early stages of lung fibrosis in IPF. When exposed to TGF-β1 and cadmium chloride, both human and rat PCLS have displayed relevant pathohistological changes commonly observed in the early phases of lung fibrosis.
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic disease where the lining of the lungs become thickened and scarred. [15] Increased ROCK activity has been found in the lungs of humans and animals with IPF. Treatment with belumosudil reduced lung fibrosis in a bleomycin mouse model study. [16]
Lanifibranor is a pan-PPAR (peroxisome proliferator-activated receptor) receptor agonist and is the first medication that targets PPAR-alpha, PPAR-beta, and PPAR-gamma simultaneously.
However, he soon found that there were major limitation of mouse models to study CF. He later found that the ferrets represent a much better model for lung disease and in 2006 his laboratory became the first in the world to clone ferrets. [4] Dr. Engelhardt's research has been geared towards finding gene therapies for cystic fibrosis.
A major driver of fibroblast activation is TGF-β [38] and as αvβ6 expression is increased in response to tissue damage, [26] and is a principal activator of TGF-β, it is therefore a potential drug target in treating fibrosis. αvβ6 can promote fibrosis in kidney, lung and skin, despite αvβ6 being almost absent in their healthy equivalents.
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