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Background <p>Postoperative complications persist in acute DeBakey type I aortic dissection (AD) despite surgical advances, yet the underlying metabolic mechanisms remain unexplored. This knowledge gap critically limits targeted interventions.</p> Methods <p>Untargeted metabolomics using ultra-high-performance liquid chromatography-mass spectrometry (UHPLC-MS) was performed on 90 serum samples, including: preoperative AD patients (<i>n</i> = 30), postoperative samples from the same cohort (AT group, <i>n</i> = 30), and healthy controls (HC, <i>n</i> = 30). Multivariate statistics through orthogonal partial least squares-discriminant analysis (OPLS-DA) identified differential metabolites (variable importance in projection [VIP] &gt; 1, <i>P</i> &lt; 0.05), with Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment revealing regulatory networks.</p> Results <p>Three interconnected mechanisms were identified: Lipid homeostasis remodeling was characterized by activated linoleic acid metabolism (<i>P</i> = 0.0136), which elevated anti-inflammatory epoxy-eicosatrienoic acids (EETs) and suppressed nuclear factor-kappa B (NF-κB) signaling; Energy reprogramming: Pyruvate/tricarboxylic acid (TCA) cycle intermediates synergized with arginine/nitric oxide (NO) pathway to scavenge reactive oxygen species (ROS).</p> Conclusions <p>We propose a multifaceted regulatory network centered on lipid remodeling, energy adaptation, and antioxidant defense, providing a multitarget framework for mitigating postoperative complications in AD.</p>

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Untargeted metabolomics-based elucidation of metabolic reprogramming mechanisms and pathways following aortic dissection surgery

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月22日

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  • Jun He,
  • Yuji Xiao,
  • Wanru Ma,
  • Yaoguang Feng,
  • Chengming Ding,
  • Haonan Zhang,
  • Heng Yang,
  • Zhengwen Lei

摘要

Background

Postoperative complications persist in acute DeBakey type I aortic dissection (AD) despite surgical advances, yet the underlying metabolic mechanisms remain unexplored. This knowledge gap critically limits targeted interventions.

Methods

Untargeted metabolomics using ultra-high-performance liquid chromatography-mass spectrometry (UHPLC-MS) was performed on 90 serum samples, including: preoperative AD patients (n = 30), postoperative samples from the same cohort (AT group, n = 30), and healthy controls (HC, n = 30). Multivariate statistics through orthogonal partial least squares-discriminant analysis (OPLS-DA) identified differential metabolites (variable importance in projection [VIP] > 1, P < 0.05), with Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment revealing regulatory networks.

Results

Three interconnected mechanisms were identified: Lipid homeostasis remodeling was characterized by activated linoleic acid metabolism (P = 0.0136), which elevated anti-inflammatory epoxy-eicosatrienoic acids (EETs) and suppressed nuclear factor-kappa B (NF-κB) signaling; Energy reprogramming: Pyruvate/tricarboxylic acid (TCA) cycle intermediates synergized with arginine/nitric oxide (NO) pathway to scavenge reactive oxygen species (ROS).

Conclusions

We propose a multifaceted regulatory network centered on lipid remodeling, energy adaptation, and antioxidant defense, providing a multitarget framework for mitigating postoperative complications in AD.