ArticleActa pharmaceutica Sinica. B2026
CD74 deficiency protects against doxorubicin cardiotoxicity through RRM2-mediated regulation of ferroptosis.
Article in Acta pharmaceutica Sinica. B, 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
Doxorubicin (DOX)-induced cardiotoxicity (DIC) is a major health threat that limits its clinical application. While mitochondrial dysfunction, oxidative stress and ferroptosis are implicated in DIC pathology, the precise mechanism remains elusive. This study evaluated the role of cluster of differentiation 74 (CD74), an immunoregulatory protein, in DIC. Our findings revealed elevated CD74 levels in blood samples from DOX-exposed patients and DOX-challenged mouse hearts. CD74 deletion mitigated DOX-indued cardiac remodeling, contractile anomaly, mitochondrial abnormalities, apoptosis, and ferroptosis. Mechanistically, CD74 bound to DNA synthesis molecule ribonucleotide reductase M2 (RRM2), redistributing it from cytoplasm to plasma membrane, impairing DOX-induced repair and exacerbating mitochondrial injury, apoptosis, and ferroptosis
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