I have been going through the Rhodes medical physiology and have learned about Endothelin (specifically its role in hyperplasia) and collateral vessels in slowly developed [cardiovascular disease] (CVD). This makes me wonder the following things:
- Why can we not avoid the scar tissue formation that plagues myocardial infarction (MI) survivors by administering Endothelin in a selective manner so as to make it only hit the type A receptors ?
- How plastic are heart cells?
FYI: I have no idea how the heart controls its plasticity and cell growth, but given that cancers in the heart are so rare surely the administration of endothelin would be well regulated