Lately I've been doing some digging around in relation to idiopathic
pulmonary fibrosis and chronic heart failure. To my surprise
osteopontin is upregulated in both cases and is now being perceived as
a primary driver of fibrosis. It is known that aldosterone increases
osteopontin production (MR specific antagonists are very efficacious in
chronic heart failure) but I'm looking for other possible causes of
increased osteopontin production because it is doubtful that it is the
causative factor in relation to idiopathic pulmonary fibrosis. Possible
targets are:
tgf beta
il-1
tnfa
Smad 3 or 7???
Can anyone here help me?
John.
