Zhang Bo-Tao, Guo Mao, Yang Liu-Rui, Zeng Yang, Jiang Jun
Department of Pain Management, Luzhou People's Hospital, Luzhou, China.
Department of General Surgery (Thyroid Surgery), The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Cancer Med. 2025 Jul;14(13):e71030. doi: 10.1002/cam4.71030.
To investigate the mechanistic aspects of inflammation and oxidative stress and their association with thyroid cancer risk.
We have systematically searched the PubMed and Web of Science databases to perform a comprehensive analysis of the pathogenic mechanisms that link obesity, inflammation, and oxidative stress to thyroid cancer.
Chronic inflammation, a well-known risk factor for cancer progression, is a hallmark characteristic of obesity. Multiple mechanisms may mediate the association between thyroid cancer and obesity. As a crucial endocrine organ, adipose tissue regulates tumor behavior, inflammation, and the tumor microenvironment through adipokines, including leptin, adiponectin, as well as chemokines. Excessive fat accumulation leads to an increase in pro-inflammatory factors, which in turn result in systemic inflammation that can further influence tumor growth and development. Oxidative stress, characterized by an imbalance between the production of reactive oxygen species (ROS) and their elimination by antioxidants, can potentially result in cellular damage and destruction. With the accumulation of ROS, it participates in numerous diseases, such as cancer and inflammation. The inflammatory condition of the thyroid gland serves as a classical source of ROS, which may, in turn, promote the development of thyroid tumors.
While various mechanisms may elucidate the relationship between inflammation, oxidative stress, and the risk of thyroid cancer, the interplay among these factors is intricate and cannot be solely attributed to a singular pathway. This review provides further insight into a strategy for the prevention and treatment of thyroid cancer, highlighting the significance of combinatorial approaches that target multiple pathways in antitumor therapy.
探讨炎症和氧化应激的作用机制及其与甲状腺癌风险的关联。
我们系统检索了PubMed和Web of Science数据库，以全面分析将肥胖、炎症和氧化应激与甲状腺癌联系起来的致病机制。
慢性炎症是癌症进展的一个众所周知的危险因素，是肥胖的一个标志性特征。多种机制可能介导甲状腺癌与肥胖之间的关联。作为一个关键的内分泌器官，脂肪组织通过脂肪因子（包括瘦素、脂联素以及趋化因子）调节肿瘤行为、炎症和肿瘤微环境。过多的脂肪堆积导致促炎因子增加，进而导致全身炎症，这可能进一步影响肿瘤的生长和发展。氧化应激的特征是活性氧（ROS）的产生与其被抗氧化剂清除之间的失衡，可能导致细胞损伤和破坏。随着ROS的积累，它参与多种疾病，如癌症和炎症。甲状腺的炎症状态是ROS的一个典型来源，反过来可能促进甲状腺肿瘤的发展。
虽然各种机制可能阐明炎症、氧化应激与甲状腺癌风险之间的关系，但这些因素之间的相互作用错综复杂，不能仅仅归因于单一途径。本综述为甲状腺癌的预防和治疗策略提供了进一步的见解，强调了在抗肿瘤治疗中针对多种途径的联合方法的重要性。
