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"Furthermore, MYSM1 mediated ferroptosis in cardiomyocytes to promote DOX-induced cardiotoxicity.A single zinc metalloprotease family is represented by the JAMMs family, whereas the remaining DUB families belong to the cysteine peptidases family [4]."

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"We have thus far focused on the compromised HSC function due to MYSM1 deficiency causing reduced protein synthesis and increased ferroptosis, as a result."

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"Consequently, we propose that MYSM1 may serve as a more viable therapeutic target than TRIM21 for addressing DOX-induced cardiotoxicity.In conclusion, our results showed that MYSM1 plays a deubiquitination role in regulating TRIM21 stability and mediating DOX-induced cardiomyocyte ferroptosis."

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"Furthermore, MYSM1 exacerbated DOX-induced cardiotoxicity by enhancing ferroptosis."

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"MYSM1 mediates ferroptosis in DOX-induced cardiotoxicity."

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"Knockdown of MYSM1 induced an increase in Nrf2 translocation from the cytosol to the nucleus (Fig. 7K), whereas overexpression of MYSM1 reversed this alteration (Fig. 7L), suggesting that MYSM1 may mediate ferroptosis through Nrf2."

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"Recent studies demonstrated that MYSM1 deficiency causes human hematopoietic stem cell loss by ferroptosis, highlighting the broader developmental and regenerative role of ferroptosis (Zhao et al., 2023)."