CCL2 and fibrosis: Besides, application of strain to human fibroblasts in vitro demonstrated that FAK acted through extracellular-related kinase (ERK) to mechanically trigger the secretion of MCP-1, a potent chemokine linked to human fibrosis, and inhibition of either FAK or ERK blocked strain-induced MCP-1 secretion, indicating that mechanical force regulated pathologic scar formation through inflammatory FAK-ERK-MCP-1 pathways (Figure 2C) (60).