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Oxidative modifications of Aβ further enhance its aggregation propensity and toxicity [9], establishing a feed-forward cycle between oxidative stress and amyloid pathology

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Furthermore, AS-IV treatment leads to a reduction in the expression levels of TGF-β1 and phosphorylated (p-)Smad3 while promoting the activation of Smad7 and intervention in rat neonatal CFs also shows a similar antifibrotic effect, indicating that the key mechanism for AS-IV to alleviate cardiac fibrosis may be the regulation of the miR-135a-TRPM7-TGF-β/Smads axis