Renal fibrosis is the final pathological process common to any ongoing, chronic kidney injury or maladaptive repair. Renal fibrosis is considered to be closely related to various cell types, such as fibroblasts, myofibroblasts, T cells, and other inflammatory cells. Multiple types of cells regulate renal fibrosis through the recruitment, proliferation, and activation of fibroblasts, and the production of the extracellular matrix. Cell trafficking is orchestrated by a family of small proteins called chemokines. Chemokines are cytokines with chemotactic properties, which are classified into 4 groups: CXCL, CCL, CX3CL, and XCL. Similarly, chemokine receptors are G protein-coupled seven-transmembrane receptors classified into 4 groups: XCR, CCR, CXCR, and CX3CR. Chemokine receptors are also implicated in the infiltration, differentiation, and survival of functional cells, triggering inflammation that leads to fibrosis development. In this review, we summarize the different chemokine receptors involved in the processes of fibrosis in different cell types. Further studies are required to identify the molecular mechanisms of chemokine signaling that contribute to renal fibrosis.
Keywords: Chemokine receptors; Macrophages; Myofibroblasts; Renal fibrosis; T cells.