Key result
Doxorubicin promotes endoplasmic reticulum stress and inflammation through iNOS/NO-induced TLR2 activation, leading to cardiomyocyte death, which is inhibited by NOS inhibitors.
Why the study?
The subcellular basis of doxorubicin-induced cardiomyopathy remains elusive despite extensive study.
Comparison
In vivo doxorubicin treatment with or without NO donor (SNAP) and/or NOS inhibitor (L-NAME)
Design
In vivo experimental study
Authors
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iNOS/NO inhibition attenuates doxorubicin cardiotoxicity in animals; leaves open translation to human cardioprotection.
Inhibition of iNOS/NO attenuates doxorubicin-induced endoplasmic reticulum stress and inflammation, highlighting a potential mechanistic target to prevent doxorubicin-induced cardiomyopathy.
Bagchi et al. (2021) studied Doxorubicin-induced cardiomyopathy. Doxorubicin and NOS inhibitors was evaluated on Endoplasmic reticulum stress, inflammation, and apoptotic responses. Doxorubicin promotes endoplasmic reticulum stress and inflammation through iNOS/NO-induced TLR2 activation, leading to cardiomyocyte death, which is inhibited by NOS inhibitors.
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