From what I remember, Revascor is likely to work by halting / slowing heart disease from progressing any further, not by remodelling the heart. If it were successful in remodelling the heart then you would've seen a decrease in hospitalisations due to decompensated heart failure, and possibly also atrial fibrillation, with the latter being more difficult to achieve. There are two major caveats when it comes to using Revascor to remodel the heart: 1) since the cells are delivered via a intramyocardial injection, some/most are lost. The cells that are retained may also only have a limited life span before they die, but are able to secrete certain factors that act locally, and 2) the dead / scar tissue that is present in the heart needs to be removed before the remodelling process can begin, which is currently not possible from what I understand.
In terms of the MOA, it is definitely inflammation-related. So why would you inject these cells into the heart muscle and not intravenously? In order to halt / slow heart disease you need to act on the local inflammatory process that is taking place in the heart. If you read up on myocardial infarction you will find that immune cells are recruited to the heart to initiate several inflammatory-related processes that eventually results in fibrosis i.e. scar tissue formation, a process that can take many, many months. Revascor cannot reverse fibrosis (currently nothing can), but it appears MPC's can act locally in the heart to stop the immune cells still in the heart from causing further damage. MPC's act by secreting paracrine factors that may also act on local cardiac tissue, fibroblasts or other cardiac stem cells to aid in repair.
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