Key result
Follistatin-like 1 (FSTL1) overexpression prevented doxorubicin-related cardiac injury, inhibited oxidative stress and apoptosis, and improved cardiac function in mice via upregulation of Nrf2.
Why the study?
Doxorubicin-induced cardiotoxicity lacks effective drug treatments, and the effect of FSTL1 on doxorubicin-induced cardiomyopathy has not been elucidated.
Does FSTL1 overexpression prevent doxorubicin-induced cardiotoxicity in mice?
Does FSTL1 overexpression prevent doxorubicin-induced cardiotoxicity in mice?
FSTL1 protects against doxorubicin-induced cardiomyopathy in preclinical models through the upregulation of Nrf2, highlighting a potential therapeutic pathway.
No takes yet. Share an insight, caveat, or question.
Should not yet change practice; leaves open human translation of FSTL1-Nrf2 targeting for doxorubicin cardioprotection.
Zhao et al. (2020) studied Doxorubicin-induced cardiomyopathy. Follistatin-like 1 (FSTL1) overexpression was evaluated on Cardiac injury, oxidative stress, apoptosis, and cardiac function. Follistatin-like 1 (FSTL1) overexpression prevented doxorubicin-related cardiac injury, inhibited oxidative stress and apoptosis, and improved cardiac function in mice via upregulation of Nrf2.
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