scarlet1967 wrote: This is another proteomic (effect of proteins) therapeutic effect of Egrifta in liver fibrosis, NAFLD and liver cancer.
As per the study angiogenesis (the development of new blood vessels) causes progression of liver fibrosis, anyone interested please look it up as it is a complex cascade of molecular reactions which is behind the theory. (https://www.ageb.be/Articles/Volume%2083%20(2020)/Fasc2/10-Lefere.pdf ).
The pro inflammatory enzymes such as VEGF and TGFB are proangiogenic proteins which also are inhibited by Tesamorelin.
So Tesamorelin’ s transcriptomic effect directly results in less fibrosis by inhibiting the pro inflammatory enzymes and indirectly inhibits the formation of new blood vessels thus less fibrosis.
“Angiogenesis is a complex process leading to the development of new vessels from pre-existing vessels. Angiogenesis occurs under physiological conditions during normal wound healing and also in pathological contexts, such as tumorigenesis, so that antiangiogenic molecules (e.g., of Bevacizumab, an anti-vascular endothelial growth factor (VEGF) monoclonal antibody) are used in the treatment of different cancers, including HCC, according to recent guidelines.
Once the neovessel is built, a maturation step is required to make the vessel functional. During this maturation step, endothelial cells go back to a quiescent state and pericytes are recruited to surround the endothelial cells, under the action of platelet-derived growth factor (PDGF), angiopoietin-1, transforming growth factor- (TGF-) and Notch.
Angiogenesis is tightly coupled to the progression of liver fibrosis and HCC, both in NAFLD as well as other chronic liver diseases.”
https://www.mdpi.com/2077-0383/10/7/1338/htm#B18-jcm-10-01338