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<p>Doxorubicin (DOX)-induced cardiotoxicity is closely associated with oxidative stress, DNA damage, and senescence-related cardiac injury. This study evaluated the protective effects of Floralozone against DOX-induced cardiac injury and explored the associated molecular changes. Floralozone alleviated DOX-induced cardiac dysfunction, myocardial structural damage, oxidative stress, DNA damage responses, and senescence-related changes in vivo and in vitro. These protective effects were accompanied by modulation of the P2Y12–AMPKα2–ASK1–MEK3-related stress signaling axis. These findings suggest that Floralozone may protect against DOX-induced cardiac injury by suppressing oxidative stress, attenuating DNA damage responses, and reducing senescence-related signaling.</p>

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P2Y12-AMPKα2 signaling contributes to cardiomyocyte senescence in doxorubicin-induced heart failure

  • 期刊论文

  • 发表日期：

    2026年6月24日

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  • Qianqian Niu,
  • Huidan Wang,
  • Mengyao Zhao,
  • Hongdou Zhang,
  • Rui Hao,
  • Peiyao Liu,
  • Lijuan Guo,
  • Bulei Chen,
  • Yuting Xi,
  • Peng Li,
  • Yaling Yin

摘要

Doxorubicin (DOX)-induced cardiotoxicity is closely associated with oxidative stress, DNA damage, and senescence-related cardiac injury. This study evaluated the protective effects of Floralozone against DOX-induced cardiac injury and explored the associated molecular changes. Floralozone alleviated DOX-induced cardiac dysfunction, myocardial structural damage, oxidative stress, DNA damage responses, and senescence-related changes in vivo and in vitro. These protective effects were accompanied by modulation of the P2Y12–AMPKα2–ASK1–MEK3-related stress signaling axis. These findings suggest that Floralozone may protect against DOX-induced cardiac injury by suppressing oxidative stress, attenuating DNA damage responses, and reducing senescence-related signaling.