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The IFN conjugates attenuated local HSC activation in an acute liver injury model and inhibited fibrogenesis in the liver fibrosis model, with no observed IFN-related side effects

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Dysfunction of VSMCs represents a key pathological basis and an important contributor to vascular diseases

This could well account for the energy failure and widespread mitochondrial dysfunction previously observed in aspirin-treated MnSOD-deficient yeast cells, as indicated by a decreased respiratory rate, disrupted mitochondrial membrane potential, and release of cytochrome c 20