ArticleJournal of thoracic disease2026
Calycosin protects against post-myocardial infarction heart failure by activating the NRF2/HO-1 signaling pathway.
Article in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Myocardial infarction (MI) is the most common cause of heart failure (HF). Calycosin (CAL), an active component of Radix astragali, has been reported to improve HF. However, the functional effect of CAL on the progression of post-MI HF has not been extensively clarified. This study aimed to investigate whether the cardioprotective effects of CAL are related to ferroptosis. Methods: In vitro, an oxygen and glucose deprivation (OGD)-induced H9c2 cells was established. Ferroptosis activator erastin and nuclear factor erythroid 2-related factor 2 (NRF2) knockdown were used in rescue experiments. Reactive oxygen species (ROS), malondialdehyde (MDA) levels, mitochondrial membrane potential (MMP), adenosine triphosphate (ATP), and Fe Results: CAL significantly reduced ROS, MDA, and Fe Conclusions: Our findings demonstrated that CAL could ameliorate post-MI HF by attenuating oxidative stress and ferroptosis through the activation of the NRF2/HO-1 signaling pathway.
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