高血压代谢组学差异代谢物与代谢通路的研究进展

Research progress on differential metabolites and metabolic pathways in hypertension based on metabolomics

  • 摘要: 本文旨在基于血清代谢组学技术,分析原发性高血压患者差异代谢物及相关代谢通路,为高血压的早期诊断和精准治疗提供新视角。通过综述现有研究,系统总结原发性高血压患者氨基酸代谢、脂肪酸代谢、氧化应激、类固醇激素代谢及其他代谢异常等多条代谢通路的异常变化及其与血压调控的关联。原发性高血压患者存在显著的氨基酸代谢紊乱,尤其是支链氨基酸、丙氨酸和精氨酸水平与血压密切相关;短链脂肪酸的代谢紊乱可通过影响血管舒缩功能影响血压水平;氧化应激可促进血管内皮损伤与收缩;类固醇激素如醛固酮和皮质醇可通过调节肾素-血管紧张素-醛固酮系统及钠水潴留加剧高血压:多种代谢通路相互作用共同促进疾病进展。代谢紊乱在原发性高血压的发生发展中起关键作用,代谢组学分析有助于揭示其病理机制,并为早期干预和靶向治疗提供理论依据。

     

    Abstract: This review aims to analyze differential metabolites and metabolic pathways in essential hypertension based on serum metabolomics, providing new insights for early diagnosis and precise treatment. Through a comprehensive review of existing studies, this paper systematically summarized abnormalities in multiple metabolic pathways—including amino acid metabolism, fatty acid metabolism, oxidative stress, steroid hormone metabolism, and other metabolic disturbances—and their associations with blood pressure regulation. Patients with essential hypertension exhibit significant disturbances in amino acid metabolism, with levels of branched-chain amino acids, alanine, and arginine being closely associated with blood pressure. Dysregulation of short-chain fatty acid metabolism may influence blood pressure by affecting vasomotor function. Oxidative stress promotes endothelial injury and vasoconstriction. Steroid hormones such as aldosterone and cortisol may exacerbate hypertension by activating the renin-angiotensin-aldosterone system and promoting sodium and water retention. The interplay among multiple metabolic pathways collectively drives disease progression. Metabolic disorders play a critical role in the pathogenesis of essential hypertension. Metabolomic analysis helps elucidate underlying mechanisms and offers a theoretical basis for early intervention and targeted therapy.

     

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