Key result
Ibudilast attenuated ROS-mediated muscle toxicity induced by doxorubicin treatment or passive smoking by inhibiting functional interactions between TRPC3 channels and Nox2.
Why the study?
Doxorubicin induces cardiotoxicity associated with increased ROS production via TRPC3-Nox2 interactions, prompting investigation into whether ibudilast targets this complex to attenuate doxorubicin-induced systemic tissue wasting.
Does not support clinical use; extends preclinical evidence for TRPC3-Nox2 inhibition in toxicity models.
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Nishiyama et al. (2019) studied Doxorubicin-induced cytotoxicity and muscle toxicity. Ibudilast vs. Control (doxorubicin alone or passive smoking alone) was evaluated on Functional interactions between TRPC3 channels and Nox2, Nox2 protein stability, and ROS production. Ibudilast attenuated ROS-mediated muscle toxicity induced by doxorubicin treatment or passive smoking by inhibiting functional interactions between TRPC3 channels and Nox2.
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