I have read that the hypoplasia can occur in fetal hypertrophic cardiomyocytes. However, I am interested if this can be theoretically be possible in non-fetal cardiomyocytes which are hypokinetic. I think there must be some growth factors to allow this to happen. Other proposals
- lysozyme, sepsis and cardiac adrenergic neural response / NO / G protein 1
- shear-wave, vortex and refolding of proteins [2 Yuan et al.]
Sources
- 1 Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling.
- 2 Yuan. Shear-Stress-Mediated Refolding of Proteins from Aggregates and Inclusion Bodies.
How can hyperplasia be regulated in non-fetal hypokinesis?
