Great post, PGS, and I thank you for your blog discussions on these trials.
Do you think the basis for this could be endothelial expression of SERCA, or simply cardiomyocyte expression of SERCA that simply loses expression over time? I do understand at least partly the potential issues with AAV and potential carbohydrate recognition mismatch between species.
To me, the pig model data is quite telling though I have not seen a peer-reviewed presentation of the data. I agree with your thoughts here. Having said that, this SERCA isoform is one of the best ways (if not THE best) to deal with CHF if expression can be directed and exist for the long haul.
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