I would check if the AT-I receptor antagonist has lost activity due to age or storage problems, or if the serum levels are not in the target range for some reason. If it is not due to some failure of the drug, it is puzzling.
TGFbeta is a tricky cytokine. In this case there are many point of regulation. Expression of the latent TGFb1 extracellular state (small or large latent complexes). Extracellular matrix stock, activation of latent forms through many pathways, signaling through phosphorylation of Smad2-3 proteins or non Smad pathways. The relevant issue is that activation or inhibition of concrete intracellular pathways, could induce TGFb1 expression while its latent state activation is inhibited or some regulatory pathways are no being activated. Check Smad2/3 phosphorylation to measure real TGFb biological activity. Also TGFb1 signaling through ALK5 receptor and Smad2/3 or ALK1 and Smad1/5/8 could be related to the response in the context that you mentioned.
when we use ELISA for analysis total TGF beta 1 , can total TGF beta 1 with angiotensin receptor blocker (ex: irbesartan), can it be increased than without irbesartan?
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