Key result
Cardiomyocyte-specific ablation of p53 was not sufficient to prevent Doxorubicin-induced myocardial ROS/RNS generation, apoptosis, interstitial fibrosis, and perivascular fibrosis in mice.
Why the study?
Does cardiomyocyte-specific ablation of p53 prevent doxorubicin-induced cardiac fibrosis and apoptosis in mice?
Population
Conditional knockout (CKO) mouse model system harbouring inactive p53 alleles specifically in cardiomyocytes
Comparison
Single dose of Doxorubicin (20 mg/kg) vs Control mice with intact p53 alleles treated…
Design
Preclinical
Follow-up
3 or 7 days
Authors
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Cardiomyocyte p53 ablation fails to block doxorubicin cardiotoxicity in mice; hypothesis-generating for p53-independent pathways and should not yet guide therapy.
Does cardiomyocyte-specific ablation of p53 prevent doxorubicin-induced cardiac fibrosis and apoptosis in mice?
Cardiomyocyte-specific ablation of p53 does not prevent doxorubicin-induced myocardial damage, indicating the involvement of p53-independent apoptotic pathways.
Feridooni et al. (2011) studied Doxorubicin-induced cardiotoxicity. Cardiomyocyte-specific ablation of p53 vs. Control mice with intact p53 alleles was evaluated on Myocardial and perivascular apoptosis and fibrosis, and ROS/RNS levels. Cardiomyocyte-specific ablation of p53 was not sufficient to prevent Doxorubicin-induced myocardial ROS/RNS generation, apoptosis, interstitial fibrosis, and perivascular fibrosis in mice.
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