Ferritinophagy and ferroptosis in cardiovascular disease: Mechanisms and potential applications

Yuhan Qin1, Yong Qiao1, Dong Wang1

  • 1Department of Cardiology, Zhongda hospital, School of Medicine, Southeast University, Dingjiaqiao 87, Gulou district, Nanjing 210009, PR China.

Insights

Ferritinophagy and ferroptosis, linked to iron and reactive oxygen species, are key cell death pathways. This review explores their role in cardiovascular disease and potential therapeutic strategies.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathology

Background:

  • Ferroptosis is regulated cell death involving iron and reactive oxygen species (ROS) accumulation.
  • Ferritinophagy, the autophagy of ferritin mediated by NCOA4, regulates ferroptosis.
  • Both ferritinophagy and ferroptosis are increasingly implicated in cardiovascular disease development.

Purpose of the Study:

  • To provide an overview of ferritinophagy and ferroptosis mechanisms.
  • To discuss the role of these cell death pathways in cardiovascular diseases.
  • To explore potential therapeutic applications of modulators targeting these pathways.

Main Methods:

  • Literature review of research on ferritinophagy and ferroptosis.
  • Analysis of mechanisms underlying ferroptosis and ferritinophagy.
  • Synthesis of evidence linking these processes to cardiovascular pathology.

Main Results:

  • Ferritinophagy influences ferroptosis, impacting cellular iron homeostasis.
  • Dysregulation of ferritinophagy and ferroptosis contributes to cardiovascular disease progression.
  • Modulators of these pathways show promise for treating cardiovascular conditions.

Conclusions:

  • Ferritinophagy and ferroptosis are critical regulators of cell death with significant implications for cardiovascular health.
  • Understanding these pathways offers novel therapeutic avenues for cardiovascular diseases.
  • Targeting ferritinophagy and ferroptosis may provide effective treatments for ferroptosis-associated cardiovascular diseases.

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