Hi...

Hi Doc



https://www.mesoblast.com/science/mechanisms-of-action


"What are your thoughts on mechanisms behind it stabilising endothelial dysfunction?"

Mechanisms by which Rex-L stabilises endothelial dysfunction primarily include: its' potent anti-inflammatory effects, due to secretion of anti-inflammatory cytokines, macrophage 1 to macrophage 2 polarisation/conversion; and paracrine functions of MSCs including inducing the release of Nitric Oxide to help vasodilate/relax the endothelium) etc








https://www.mesoblast.com/images/pdf/Phase_3_DREAM-HF_Trial_of_MPCs_in_Chronic_HF-A_review_of_biological_plausibility__implementation_of_flexible_clinical_trial_design_CIRCULATION_RESEARCH_JULY_2019-.pdf


"And if it reduces maladaptive remodelling, why did it not have any effect on the LVEF?"

I can not comment on the above question because I have not seen data for the intervention group in regards to any changes in the LVEF. Was this even measured post-intervention? At what time frame? Please provide link if you get a chance.



I did find the above paragraph in the PDF link provided which makes me wonder if non radionucleotide imaging studies like MRI scans and echocardiography to assess the shape and size of the ventricles may be a better way to measure the extent of damage caused by ventricular remodeling.

In short Doc, my opinions do not stray too far from the science and experts like Dr Perin.