Key result
Floralozone alleviated doxorubicin-induced cardiac dysfunction, myocardial structural damage, oxidative stress, DNA damage responses, and senescence-related changes in vivo and in vitro.
Why the study?
Doxorubicin-induced cardiotoxicity is closely associated with oxidative stress, DNA damage, and senescence-related cardiac injury, motivating investigation into protective interventions.
Does Floralozone protect against doxorubicin-induced cardiac injury in preclinical models?
Does Floralozone protect against doxorubicin-induced cardiac injury in preclinical models?
Floralozone demonstrates protective effects against doxorubicin-induced cardiotoxicity in preclinical models by modulating the P2Y12-AMPKα2 signaling pathway.
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.
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Niu et al. (2026) studied Doxorubicin-induced cardiotoxicity. Floralozone was evaluated on Cardiac dysfunction, myocardial structural damage, oxidative stress, DNA damage responses, and senescence-related changes. Floralozone alleviated doxorubicin-induced cardiac dysfunction, myocardial structural damage, oxidative stress, DNA damage responses, and senescence-related changes in vivo and in vitro.
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