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Fibrosis is a pathological process characterized by the abnormal deposition of connective tissue across multiple organ systems. Given the high prevalence of fibrotic diseases and the limited availability of clinical treatment options, it has emerged as a major challenge in contemporary medicine. Chronic inflammation is widely recognized as a common pathological basis of various fibrotic disorders. In fibrosis progression, CCR2 acts as a critical signaling hub, initiating cascade reactions and contributing to the formation of a complex regulatory network. Studies have demonstrated that in most organ fibrotic processes, CCR2 primarily exerts pro-fibrotic effect by recruiting inflammatory monocytes, activating fibroblasts, and promoting extracellular matrix deposition. However, the function of CCR2 is not unidimensional. It may also play a regulatory role in promoting fibrosis regression under specific tissue and pathological contexts. CCR2 signaling exhibits dual regulatory properties at different stages of liver fibrosis. CCR2 promotes injury in the early phase, while participating in fibrosis reversal by mediating macrophage transition toward a reparative phenotype and facilitating extracellular matrix degradation. This stage-dependent behavior suggests that inappropriate timing of intervention may disrupt repair process, and the functional redundancy of the chemokine system may trigger compensatory adaptations. Together, these factors constitute the core translational challenges facing CCR2-targeted therapeutic strategies. This article systematically reviews the complex regulatory network and pivotal role of CCR2 signaling in fibrosis progression, summarizes the latest advances in the diagnosis and treatment of clinically relevant fibrotic diseases associated with this pathway, analyzes the specific challenges in translating CCR2-targeted therapies into clinical practice, and outlines future research directions.