Abstract
Chemokines are regarded as major contributors to tumor growth and inflammation. They participate in cancer progression directly and accelerate tumor microenvironment (TME) remodeling because of the inflammatory response and immune cell infiltration. C-C motif chemokine ligand 7 (CCL7) is widely expressed across various cell types. In tumors, CCL7 facilitates progression by shaping the TME and promoting cell invasion and metastasis. It also enhances anti-tumor immune responses by recruiting immune cells such as T cells and NK cells. Moreover, emerging evidence indicates that the overexpression of CCL7 is associated with inflammatory diseases. CCL7 predominantly attracts macrophages and monocytes, thereby modulating inflammatory responses, driving fibrosis progression, and maintaining systemic homeostasis. However, the exact mechanisms underlying these processes remain unclear and lack systematic investigation. This review systematically integrates CCL7's dual roles in tumors (both pro-tumor and anti-tumor) and its stage-specific functions across inflammation (both pro-inflammatory and anti-inflammatory), fibrosis, and obesity, filling gaps in fragmented prior research. It also links the common regulatory mechanisms across multiple diseases, and puts forward specific strategies such as CCL7/CCR antagonists and combined immunotherapy, thereby providing new therapeutic strategies for the exploration and treatment of related diseases, aiming to contribute to the maintenance of human health globally.