Dipeptidyl peptidases (DPPs, CD26) were first assigned a role in inflammatory disorders. One of the first inflammatory diseases in which DPPs have been found was in the synovial membrane from patients with rheumatoid arthritis, suggesting an immunological role for this group of peptidases in inflammation disturbances.
Specifically, DPP4 was found on the surface of inflamed human synovium, proposing potential approaches to the pharmacological manipulation of inflammation by specific enzyme inhibitors. Ischemia-reperfusion (I/R) injury is a form of inflammation that reflects various key features of inflammation such as tissue injury and the involvement of various immune cells. During the development of I/R injury, a plethora of proteins are involved and many of them are substrates to CD26/DPP4 cleavage. Thus, inhibiting these substrates by CD26/DPP4-inhibitors (gliptins) can potentially ameliorate inflammatory diseases.
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