尿酸
转化(遗传学)
癌症
新陈代谢
癌症研究
内科学
医学
生物化学
化学
基因
作者
Z. Li,Yu‐Wen Su,Hang Su,Jiashu Pan,Sumei Li,Lu Lu,Guang Ji,Hanchen Xu
标识
DOI:10.1016/j.jare.2025.08.031
摘要
Hyperuricemia-induced oxidative stress, DNA damage and genomic instability, while simultaneously activating proinflammatory signaling pathways. These interconnected pathways establish a persistent, proinflammatory microenvironment that fosters the transition from inflammation to cancer. Therapeutic strategies targeting UA metabolism (including pharmacologic interventions and dietary modifications) may mitigate chronic low-grade inflammation and reduce the cancer risk associated with hyperuricemia. Dysregulated UA metabolism emerges as a critical modulator linking chronic inflammation with oncogenesis.
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