Key result
Nrf2 deficiency exaggerated doxorubicin-induced cardiomyocyte necrosis and cardiac dysfunction, indicating Nrf2 acts as an endogenous suppressor of cardiotoxicity.
Population
Wild type (WT) and Nrf2 knockout (Nrf2-/-) mice, and cultured cardiomyocytes
Comparison
Doxorubicin 25 mg/kg single intraperitoneal… vs Wild type mice vs Nrf2-/- mice; control…
Design
Preclinical
Authors
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Should not alter doxorubicin regimens in patients; hypothesis-generating for Nrf2 activation in cardiotoxicity models.
Nrf2 appears to be an endogenous suppressor of doxorubicin-induced cardiotoxicity by controlling oxidative stress and autophagy.
Li et al. (2014) studied Doxorubicin-induced cardiotoxicity. Nrf2 deficiency vs. Wild type (normal Nrf2 expression) was evaluated on Doxorubicin-induced adverse effects (cardiomyocyte necrosis and cardiac dysfunction). Nrf2 deficiency exaggerated doxorubicin-induced cardiomyocyte necrosis and cardiac dysfunction, indicating Nrf2 acts as an endogenous suppressor of cardiotoxicity.
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