Key result
Forced Notch pathway activation expanded the proliferative capacity of neonatal cardiomyocytes but was largely ineffective in stimulating cardiac repair after myocardial infarction in adult mice.
Why the study?
Does forced Notch pathway activation by AAV gene transfer induce cardiac regeneration after myocardial infarction in mice?
Population
Neonatal and adult mice with myocardial infarction
Design
Preclinical
Authors
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No support for Notch activation in adult post-MI repair; leaves open epigenetic targeting to overcome age-dependent silencing.
Does forced Notch pathway activation by AAV gene transfer induce cardiac regeneration after myocardial infarction in mice?
Notch pathway activation fails to drive cardiac regeneration in adult mice after myocardial infarction due to permanent epigenetic silencing at Notch-responsive promoters.
Felician et al. (2014) studied Myocardial infarction. Adenoassociated virus gene transfer of activated Notch1 or its ligand Jagged1 was evaluated on Cardiac regeneration and cardiomyocyte proliferation. Forced Notch pathway activation expanded the proliferative capacity of neonatal cardiomyocytes but was largely ineffective in stimulating cardiac repair after myocardial infarction in adult mice.
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