Why the study?
Doxorubicin induces cardiac aging through mechanisms that remain incompletely understood, necessitating investigation of molecular regulators such as CD47.
Does ligufalimab prevent doxorubicin-induced cardiac aging and dysfunction in mice and cultured cardiomyocytes?
Does ligufalimab prevent doxorubicin-induced cardiac aging and dysfunction in mice and cultured cardiomyocytes?
CD47 blockade may offer a novel therapeutic strategy to mitigate anthracycline-induced cardiotoxicity and cardiac aging.
May prompt CD47-targeted studies in doxorubicin cardiotoxicity; leaves open any clinical role pending mechanistic validation.
Cardiac aging is a natural process that occurs with age, leading to structural and functional abnormalities of the heart. In addition to chronological age, anticancer therapies can accelerate this process. Doxorubicin, an anthracycline class antitumor drug, is known to have significant cardiac toxicity including cardiac aging, but the underlying mechanisms remain incompletely understood. In this study, we identified that CD47 was significantly increased in aged hearts through bioinformatic analyses. We next established a doxorubicin-induced cardiac aging model in mice. Doxorubicin increased p53, p16, and p21 expression in mouse hearts, accompanied by marked CD47 upregulation. Similar effects were observed in AC16 cardiomyocytes, in which doxorubicin induced CD47 expression and a senescence-like phenotype, including increased p16 and p21 levels and SA-β-gal positivity. Blocking CD47 with a specific antibody attenuated doxorubicin-induced cardiac aging and cardiomyocyte senescence in vivo and in vitro, and improved doxorubicin-induced cardiac dysfunction. These results identify CD47 as a functional mediator of doxorubicin-induced cardiac aging and support CD47 blockade as a potential strategy to mitigate anthracycline-associated cardiac dysfunction.
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Yan et al. (2026) studied Doxorubicin-induced cardiac aging. Ligufalimab (CD47 blockade) vs. Doxorubicin alone was evaluated on Cardiac function (LVEF, LVFS) and cellular senescence markers (p16, p21, p53).
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