Linking homocysteine and ferroptosis in cardiovascular disease: insights and implications

Xiaozhong Li1,2, Zheng Zhou1,2, Yu Tao1

  • 1Department of Cardiovascular Medicine, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.

Insights

Homocysteine (Hcy) contributes to cardiovascular disease (CVD) risk. This review explores how Hcy influences ferroptosis, a cell death pathway implicated in CVD, to advance understanding of disease mechanisms.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cardiovascular Medicine

Background:

  • Homocysteine (Hcy) is a methionine metabolite linked to cardiovascular disease (CVD).
  • Ferroptosis, a cell death form marked by iron and lipid peroxidation, is implicated in various diseases, including CVD.
  • The specific impact of Hcy on ferroptosis remains underexplored.

Purpose of the Study:

  • To investigate the potential roles and mechanisms of homocysteine in ferroptosis within cardiovascular disease.
  • To summarize recent findings on the effects of Hcy on ferroptosis in CVD.

Main Methods:

  • Comprehensive literature research and analysis.
  • Review of existing studies on homocysteine, ferroptosis, and cardiovascular disease.

Main Results:

  • Emerging evidence suggests a link between elevated homocysteine levels and ferroptosis induction.
  • Homocysteine may promote ferroptosis through mechanisms involving oxidative stress and iron metabolism.
  • Ferroptosis activation by homocysteine could contribute to cardiovascular tissue damage.

Conclusions:

  • Homocysteine plays a significant role in promoting ferroptosis, exacerbating cardiovascular disease pathology.
  • Understanding the Hcy-ferroptosis axis offers novel therapeutic targets for CVD.
  • Further research is needed to fully elucidate the molecular mechanisms involved.

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