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Peer-reviewedCC BY 4.0Advanced Science

Stress Hyperglycemia Drives CD4+ T Cell PANoptosis and Postoperative Organ Injury via Monocyte‐Derived Succinate

  • Shuai Zhao1,2
  • Xuemei Miao1,2
  • Wei Luo1,2
  • Tao Liu1,2
  • Yang Wang1,2
  • Jiaying Li1,2
  • Di Fu2,3
  • Weiyun Shen1,2
  • Yan Luo2
  • Kang Chen4
  • Ruping Dai1,2
  • Hui Li1,2
4 affiliations
  1. 1Department of Anesthesiology the Second Xiangya Hospital Central South University Changsha China
  2. 2Anesthesiology Research Institute of Central South University Changsha Changsha China
  3. 3Department of Anesthesiology XiangYa Hospital Central South University Changsha China
  4. 4Department of Obstetrics and Gynecology Wayne State University Detroit USA
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Abstract

Perioperative stress hyperglycemia is a transient but frequent metabolic disturbance strongly linked to postoperative organ injury and mortality; however, the immunometabolic mechanisms driving this association remain largely undefined. In a two‐center cohort of patients undergoing total aortic arch replacement, we identify stress hyperglycemia as an independent determinant of poor postoperative outcomes that associates strongly with CD4+ T cell loss. Hyperglycemia induces inflammatory PANoptosis in CD4+ T cells from patients in response to surgical trauma. This results from elevated glucose driving the accumulation and release of succinate from monocytes, which subsequently acts on CD4+ T cells to compromise mitochondrial integrity and activate ZBP1‐mediated PANoptosis. Our findings define a monocyte–T cell metabolic signaling axis that transduces hyperglycemic stress via elevated succinate to adaptive immune cell death and reveal potential therapeutic targets to prevent postoperative immune dysfunction and organ injury, especially for patients with hyperglycemic comorbidities.

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Cite

BibTeXRIS
BibTeX
@article{zhao2026stress,
  title = {{Stress Hyperglycemia Drives CD4+ T Cell PANoptosis and Postoperative Organ Injury via Monocyte‐Derived Succinate}},
  author = {Shuai Zhao and Xuemei Miao and Wei Luo and Tao Liu and Yang Wang and Jiaying Li and Di Fu and Weiyun Shen and Yan Luo and Kang Chen and Ruping Dai and Hui Li},
  journal = {Advanced Science},
  year = {2026},
  month = aug,
  doi = {10.1002/advs.76968},
  url = {https://doi.org/10.1002/advs.76968},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Stress Hyperglycemia Drives CD4+ T Cell PANoptosis and Postoperative Organ Injury via Monocyte‐Derived Succinate
AU  - Shuai Zhao
AU  - Xuemei Miao
AU  - Wei Luo
AU  - Tao Liu
AU  - Yang Wang
AU  - Jiaying Li
AU  - Di Fu
AU  - Weiyun Shen
AU  - Yan Luo
AU  - Kang Chen
AU  - Ruping Dai
AU  - Hui Li
PY  - 2026
DA  - 2026/08/05
JO  - Advanced Science
DO  - 10.1002/advs.76968
UR  - https://doi.org/10.1002/advs.76968
AB  - Perioperative stress hyperglycemia is a transient but frequent metabolic disturbance strongly linked to postoperative organ injury and mortality; however, the immunometabolic mechanisms driving this association remain largely undefined. In a two‐center cohort of patients undergoing total aortic arch replacement, we identify stress hyperglycemia as an independent determinant of poor postoperative outcomes that associates strongly with CD4+ T cell loss. Hyperglycemia induces inflammatory PANoptosis in CD4+ T cells from patients in response to surgical trauma. This results from elevated glucose driving the accumulation and release of succinate from monocytes, which subsequently acts on CD4+ T cells to compromise mitochondrial integrity and activate ZBP1‐mediated PANoptosis. Our findings define a monocyte–T cell metabolic signaling axis that transduces hyperglycemic stress via elevated succinate to adaptive immune cell death and reveal potential therapeutic targets to prevent postoperative immune dysfunction and organ injury, especially for patients with hyperglycemic comorbidities.
SN  - 2198-3844
ER  -