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<p>Aortic dissection (AD), characterized by rupture of the aortic wall, presents significant diagnostic challenges due to its rapid onset and nonspecific clinical symptoms. Although conventional imaging techniques are clinically useful, they typically lack sensitivity for early AD detection, are often unavailable in resource-limited settings, and cannot elucidate the mechanistic basis of AD pathogenesis. In this study, we used metabolomics and lipidomics to analyze serum samples from healthy controls, hypertensive AD patients, and normotensive AD patients, revealing distinct metabolic and lipidomic perturbations associated with AD, independent of blood pressure status. Notably, mitochondrial dysfunction was a pivotal factor in AD pathogenesis, and key metabolites such as acetylcarnitine served as both an AD biomarker and an indicator of disrupted lipid metabolism. Lipidomic profiling further revealed a consistent accumulation of specific fatty acids in AD patients, including elevated levels of FA(16:1), FA(20:1), FA(22:5), and FA(20:2) in both hypertensive and normotensive subgroups. Additionally, the sphingolipid signaling pathway was the most markedly altered lipidomic pathway between the two AD groups. These findings offer new insights into the complex lipidomic and metabolic mechanisms underlying AD pathogenesis, paving the way for improved diagnostics and targeted therapeutic strategies.</p>

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Integrated metabolomics and lipidomics reveal fatty acid dysregulation in aortic dissection independent of hypertension

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月14日

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  • Xuanxuan Bai,
  • Hongbin Lin,
  • Weiliang Zheng,
  • Lijun Sun,
  • Shuangkun Chen,
  • Lin Lu,
  • Lulu Chen,
  • Xijie Wu

摘要

Aortic dissection (AD), characterized by rupture of the aortic wall, presents significant diagnostic challenges due to its rapid onset and nonspecific clinical symptoms. Although conventional imaging techniques are clinically useful, they typically lack sensitivity for early AD detection, are often unavailable in resource-limited settings, and cannot elucidate the mechanistic basis of AD pathogenesis. In this study, we used metabolomics and lipidomics to analyze serum samples from healthy controls, hypertensive AD patients, and normotensive AD patients, revealing distinct metabolic and lipidomic perturbations associated with AD, independent of blood pressure status. Notably, mitochondrial dysfunction was a pivotal factor in AD pathogenesis, and key metabolites such as acetylcarnitine served as both an AD biomarker and an indicator of disrupted lipid metabolism. Lipidomic profiling further revealed a consistent accumulation of specific fatty acids in AD patients, including elevated levels of FA(16:1), FA(20:1), FA(22:5), and FA(20:2) in both hypertensive and normotensive subgroups. Additionally, the sphingolipid signaling pathway was the most markedly altered lipidomic pathway between the two AD groups. These findings offer new insights into the complex lipidomic and metabolic mechanisms underlying AD pathogenesis, paving the way for improved diagnostics and targeted therapeutic strategies.