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Peer-reviewedCC BYJournal of diabetes

Txnip/PDK4-Mediated Hyperdependence on Fatty-Acid Oxidation Amplifies Susceptibility of Diabetic Myocardium to Ischemia-Reperfusion Damage.

  • Zheng Zeng1
  • Wei Shi2
  • Yuxuan He1
  • Yue Wang1
  • Cong Pu1
  • Jingtong Tan1
  • Hai Guo1
  • Haiping Ma1
  1. 1Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China.
  2. 2Catheterization Laboratory, Changji Prefecture People's Hospital, Changji Hui Autonomous Prefecture, Xinjiang, China.
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Abstract

Background

Undergoing perioperative ischemia-reperfusion injury (I/RI), the prevalence of adverse cardiac events is high due to increased myocardial vulnerability in diabetic patients. However, the specific mechanisms of increased myocardial vulnerability in diabetes are still unknown.Objective

To investigate the specific mechanisms underlying increased myocardial vulnerability in diabetes and to explore potential myocardial protective strategies.Methods

In this study, we repeatedly verified through single-cell sequencing, fluorescence in situ staining, metabonomics, and animal experiments.Results

Here we show for the first time that the cardiomyocyte subtype (C6 cardiomyocyte) is a cardiomyocyte characterized by myocardial contraction, and the reduction of its number and metabolic heterogeneity is the basis of myocardial ischemia-reperfusion injury in diabetes. Among them, TXNIP/PDK4 mediated metabolic reprogramming is an important reason for myocardial vulnerability in diabetes, and through regulating TXNIP/PDK4, we optimize myocardial energy metabolism. It can significantly improve the vulnerability of diabetes myocardium, play a good role in myocardial protection, and has clinical transformation potential.

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Cite

BibTeXRIS
BibTeX
@article{zeng2026txnippdk4mediated,
  title = {{Txnip/PDK4-Mediated Hyperdependence on Fatty-Acid Oxidation Amplifies Susceptibility of Diabetic Myocardium to Ischemia-Reperfusion Damage.}},
  author = {Zheng Zeng and Wei Shi and Yuxuan He and Yue Wang and Cong Pu and Jingtong Tan and Hai Guo and Haiping Ma},
  journal = {Journal of diabetes},
  year = {2026},
  month = oct,
  doi = {10.1111/1753-0407.70277},
  url = {https://europepmc.org/article/MED/42899436},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Txnip/PDK4-Mediated Hyperdependence on Fatty-Acid Oxidation Amplifies Susceptibility of Diabetic Myocardium to Ischemia-Reperfusion Damage.
AU  - Zheng Zeng
AU  - Wei Shi
AU  - Yuxuan He
AU  - Yue Wang
AU  - Cong Pu
AU  - Jingtong Tan
AU  - Hai Guo
AU  - Haiping Ma
PY  - 2026
DA  - 2026/10/01
JO  - Journal of diabetes
DO  - 10.1111/1753-0407.70277
UR  - https://europepmc.org/article/MED/42899436
AB  - Background  Undergoing perioperative ischemia-reperfusion injury (I/RI), the prevalence of adverse cardiac events is high due to increased myocardial vulnerability in diabetic patients. However, the specific mechanisms of increased myocardial vulnerability in diabetes are still unknown.Objective  To investigate the specific mechanisms underlying increased myocardial vulnerability in diabetes and to explore potential myocardial protective strategies.Methods  In this study, we repeatedly verified through single-cell sequencing, fluorescence in situ staining, metabonomics, and animal experiments.Results  Here we show for the first time that the cardiomyocyte subtype (C6 cardiomyocyte) is a cardiomyocyte characterized by myocardial contraction, and the reduction of its number and metabolic heterogeneity is the basis of myocardial ischemia-reperfusion injury in diabetes. Among them, TXNIP/PDK4 mediated metabolic reprogramming is an important reason for myocardial vulnerability in diabetes, and through regulating TXNIP/PDK4, we optimize myocardial energy metabolism. It can significantly improve the vulnerability of diabetes myocardium, play a good role in myocardial protection, and has clinical transformation potential.
SN  - 1753-0393
SN  - 1753-0407
ER  -