2. Academic Validation
  3. SLC1A5 mediates myocardial damage after myocardial infarction by triggering cardiomyocyte ferroptosis

SLC1A5 mediates myocardial damage after myocardial infarction by triggering cardiomyocyte ferroptosis

  • Biochem Pharmacol. 2025 Sep:239:117047. doi: 10.1016/j.bcp.2025.117047.
Dong Wang 1,  Lei Li 2,  Feng Zhang 2,  Qian Liu 2,  Wen-Long Wang 2,  Zhi-Xin Wang 2,  Yu-Ting Wu 3,  Pei-Li Bu 4
Affiliations

Affiliations

  • 1 State Key Laboratory for Innovation and Transformation of Luobing Theory; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province; Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China; Binzhou Medical University Hospital, Binzhou 256603, China.
  • 2 Binzhou Medical University Hospital, Binzhou 256603, China.
  • 3 Binzhou Medical University Hospital, Binzhou 256603, China; School of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China. Electronic address: 1603406288@qq.com.
  • 4 State Key Laboratory for Innovation and Transformation of Luobing Theory; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province; Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China. Electronic address: bupeili@outlook.com.
PMID: 40490039 DOI: 10.1016/j.bcp.2025.117047
Abstract

Myocardial infarction (MI) has become a major disease that causes significant global mortality. Notably Ferroptosis may exert a key effect on myocardial injury after MI. As the glutamine transporter on the cell membrane, solute carrier family 1 member 5 (SLC1A5) plays a role as a ferroptosis-inducing gene and has a mediating effect on cell Ferroptosis. However, whether SLC1A5 is involved in mediating cardiomyocyte Ferroptosis and myocardial injury after MI remains to be further elucidated. In the present study, we investigated whether SLC1A5 mediated myocardial injury after MI by triggering cardiomyocyte Ferroptosis in vivo and in vitro. Based on our findings, SLC1A5 exhibited crucial mediating effects on post-MI cardiomyocyte Ferroptosis and myocardial injury, and these effects were stimulated by SLC1A5 overexpression, but inhibited by ferrostatin-1 (a Ferroptosis inhibitor)and V9302 (a SLC1A5 inhibitor). In conclusion, our results revealed a novel molecular mechanism of Ferroptosis regulated by SLC1A5, which is essential for cardiomyocyte Ferroptosis pathogenesis and myocardial injury post-MI.

Keywords

Ferroptosis; Myocardial infarction; SLC1A5.

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