Tectorigenin Protects Irradiation-Induced Injury of HUVECs by Inhibiting Mitophagy Through PINK1/Parkin Pathway

  • Front Biosci (Landmark Ed). 2026 May 25;31(5):48938. doi: 10.31083/FBL48938.
Chenxi Liu  1  2 ,  Fengsheng Li  3 ,  Wen Wen  2 ,  Mingyue Qu  4 ,  Chao Yang  5 ,  Zhitao Jin  1 ,  Jiaojiao Xu  2 ,  Xiaojiong Lu  6 ,  Zheng Zhang  1
Affiliations
  • 1. Department of Cardiology, Chinese People's Liberation Army Rocket Force Characteristic Medical Center, 100088 Beijing, China.
  • 2. The Graduate Training Base of Jinzhou Medical University, Department of Cardiology, Chinese People's Liberation Army Rocket Force Characteristic Medical Center, 100088 Beijing, China.
  • 3. Department of Nuclear Radiation Injury and Monitoring, Chinese People's Liberation Army Rocket Force Characteristic Medical Center, 100088 Beijing, China.
  • 4. Medical Research Department, Chinese People's Liberation Army Rocket Force Characteristic Medical Center, 100088 Beijing, China.
  • 5. Department of General Medicine, Chinese People's Liberation Army Rocket Force Characteristic Medical Center, 100088 Beijing, China.
  • 6. Department of Respiratory Medicine, Chinese People's Liberation Army Rocket Force Characteristic Medical Center, 100088 Beijing, China.
PMID: 42216527 DOI: 10.31083/FBL48938
Abstract

Objective: This study aimed to investigate the protective effect of Tectorigenin against irradiation-induced endothelial cell damage and to elucidate the underlying mechanism, thereby identifying potential therapeutic targets for irradiation-induced heart disease.

Methods: An in vitro radiation-induced injury model was established to evaluate oxidative stress and Apoptosis. Mitochondrial morphology was assessed by transmission electron microscopy, while mitochondrial function was evaluated using JC-1 staining, MitoSOX staining, immunofluorescence, and ATP assays. To investigate the involvement of Mitophagy in the underlying mechanism, a Mitophagy inhibitor, PINK1 siRNA, and PINK1 overexpression were employed.

Results: Tectorigenin significantly attenuated radiation-induced oxidative stress and Apoptosis, suppressed mitochondrial Reactive Oxygen Species (ROS) generation and membrane depolarization, and attenuated Mitophagy activation through downregulation of PINK1 and Parkin expression. Notably, PINK1 inhibition potentiated these protective effects, whereas PINK1 overexpression abrogated Tec-mediated protection.

Conclusion: Tectorigenin alleviated irradiation-induced injury through suppressing the activation of PINK1-mediated Mitophagy, thereby offering potential therapeutic targets and candidate agents for radiation-induced heart disease (RIHD).

Keywords
PINK1/Parkin; gene regulation; irradiation; mitophagy; tectorigenin.
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