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Moreover, BA treatment protects against ATO-induced cardiotoxicity by suppressing oxidative stress, inflammatory factor expression, and by enhancing endogenous antioxidant systems through the inhibition of the TLR4/NF-B signaling pathway [254]

Inhibition of miRNA binding improved cardiac function and restored mitochondrial fatty acid oxidation in animal models, thus highlighting a novel potential therapy for heart failure (36)

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Ein Beitrag zur Klinik und pathologischen Anatomie der Westphal-Struempellschen Pseudosklerose