Key result
Adiponectin protected against doxorubicin-induced cardiotoxicity by improving left ventricle dysfunction and reducing myocardial apoptosis through an Akt-dependent mechanism.
Why the study?
Does adiponectin ameliorate doxorubicin-induced cardiotoxicity in preclinical models?
Population
Adiponectin knock-out and wild-type mice, Akt1 heterozygous KO mice, and cultured rat neonatal cardiomyocytes.
Comparison
Systemic delivery of adenoviral vector… vs Wild-type mice, untreated controls, or APN-KO…
Design
Preclinical
Authors
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Hypothesis-generating for adiponectin-Akt signaling in doxorubicin cardiotoxicity; leaves open translation to clinical cardioprotection.
Does adiponectin ameliorate doxorubicin-induced cardiotoxicity in preclinical models?
Adiponectin protects against doxorubicin-induced cardiotoxicity via an Akt protein-dependent mechanism, highlighting a potential pathway to mitigate chemotherapy-induced heart failure.
Maruyama et al. (2011) studied Doxorubicin-induced cardiotoxicity. Adiponectin vs. Wild-type or untreated controls was evaluated on Mortality, left ventricle contractile dysfunction, and myocardial apoptosis. Adiponectin protected against doxorubicin-induced cardiotoxicity by improving left ventricle dysfunction and reducing myocardial apoptosis through an Akt-dependent mechanism.
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