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Fibrosis is a pathological process caused by abnormal wound healing response, which often leads to excessive deposition of extracellular matrix, distortion of organ architecture, and loss of organ function. Aging is an important risk factor for the development of organ fibrosis. C-X-C receptor 4 (CXCR4) is the predominant chemokine receptor on fibrocytes, C-X-C motif ligand 12 (CXCL12) is the only ligand of CXCR4. Accumulated evidence have confirmed that CXCL12/CXCR4 can be involved in multiple pathological mechanisms in fibrosis, such as inflammation, immunity, epithelial-mesenchymal transition, and angiogenesis. In addition, CXCL12/CXCR4 have also been shown to improve fibrosis levels in many organs including the heart, liver, lung and kidney; thus, they are promising targets for anti-fibrotic therapy. Notably, inhibitors of CXCL12 or CXCR4 also play an important role in various fibrosis-related diseases. In summary, this review systematically summarizes the role of CXCL12/CXCR4 in fibrosis, and this information is of great significance for understanding CXCL12/CXCR4. This will also contribute to the design of further studies related to CXCL12/CXCR4 and fibrosis, and shed light on potential therapies for fibrosis. • Fibrosis is a typical aging-related pathological process, and is regarded as a common pathway to organ injury and failure. • CXCL12/CXCR4 have different effects on fibrogenesis, including inflammation, immunity, epithelial-mesenchymal transition, and angiogenesis. • CXCL12/CXCR4 are involved in fibrosis in various organs, including the heart, liver, lung, and kidney. • It is of great clinical importance to further explore the effect of CXCL12/CXCR4 inhibition to potentiate the clinical effectiveness. [ABSTRACT FROM AUTHOR]