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:

  1. 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 ?
  2. 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

  • Would you mind rephrasing the question title? I'm trying to get my mind work out the meaning, but it's hard to understand.
    – Narusan
    Commented Jun 17, 2017 at 22:35
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    Sure thing, my english isnt great but ive reworded the quesiton Commented Jun 17, 2017 at 23:05
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    I have proposed an edit which spells out acronyms, fixes some language problems and links medical terminology to articles. Feel free to accept or reject it.
    – Narusan
    Commented Jun 27, 2017 at 11:59
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    Thanks - You see, that's the issue with acronyms: You meant cardiovascular disease, and I thought of chemical vapor deposition, although I should have guessed it from the context.
    – Narusan
    Commented Jun 27, 2017 at 14:02
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    I'm voting to close this question as off-topic because it's a theoretical question. Commented Mar 11, 2018 at 6:08

1 Answer 1

  1. It seems to be still under debate. Contradictory evidence has been found.

The relative importance of Endothelin Type A and Endothelin Type B receptors during myocardial ischaemia are still debated.

  1. The word you are seeking is regenerative. Mammalian hearts are made from non-regenerative tissue.

"While several animals can regenerate heart damage (e.g. the axolotl), mammalian cardiomyocytes (heart muscle cells) cannot proliferate (multiply) and heart damage causes scarring and fibrosis."

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