Mechanistic insights into lipoprotein(a)-induced cardiomyocyte ferroptosis via ROS/p38/p53 signaling - Takeaways - MDSpire

Mechanistic insights into lipoprotein(a)-induced cardiomyocyte ferroptosis via ROS/p38/p53 signaling

  • By

  • Yujia Li

  • Xi Chen

  • Chuan He

  • Yukai Zhang

  • Tiechao Jiang

  • July 13, 2026

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  • 1

    Lipoprotein(a) [Lp(a)] is linked to cardiovascular risk and induces ferroptosis in cardiomyocytes through redox-sensitive pathways.

  • 2

    Lp(a) exposure leads to increased intracellular Fe2+ and malondialdehyde levels, indicating ferroptotic events in cardiomyocytes.

  • 3

    p38 MAPK activation is central to Lp(a)-induced ferroptosis, as pharmacological blockade significantly reduces ferroptotic markers.

  • 4

    Lp(a) promotes reactive oxygen species (ROS) accumulation, activating p38 and subsequently p53, which inhibits SLC7A11 expression.

  • 5

    In vivo studies in Lp(a)-treated mice confirmed cardiac dysfunction and ferroptotic markers, validating the in vitro findings.

Original Source(s)

Mechanistic insights into lipoprotein(a)-induced cardiomyocyte ferroptosis via ROS/p38/p53 signaling

  • by Yujia Li, Xi Chen, Chuan He, Yukai Zhang, Tiechao Jiang

  • July 13, 2026

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