Obesity is a chronic metabolic disorder that is closely associated with the occurrence and progression of breast cancer. Recent studies have shown that chronic low-grade inflammation may be an important mechanism linking between obesity and breast cancer. In the obese state, adipose tissue expansion and dysfunction promote the infiltration of inflammatory cells, particularly macrophages, leading to the persistent release of pro-inflammatory factors such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), thereby establishing a chronic inflammatory microenvironment. In addition, obesity can further promote breast cancer through multiple mechanisms, including enhanced aromatase expression, increased estrogen biosynthesis, insulin resistance, and dysregulation of adipokine secretion. The inflammation-related signaling pathways, including IL-6/STAT3, TNF-α/NF-κB, and the NLRP3 inflammasome, play pivotal roles in tumor cell proliferation, epithelial-mesenchymal transition, angiogenesis, and immune evasion. Furthermore, obesity‑driven adipose tissue inflammation remodels the tumor immune microenvironment, thereby augmenting the invasive and metastatic capacity of breast cancer. Therefore, regulating obesity-related chronic inflammation and its metabolic abnormalities is expected to be an important strategy for breast cancer prevention and intervention. This review summarizes the current advances in the mechanisms and signaling pathways through which obesity-associated chronic inflammation contributes to breast cancer development and progression, aiming to provide a theoretical basis for precision prevention and targeted therapy of breast cancer.
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Research progress on obesity, chronic inflammation and breast cancer risk
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