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Targeting CD26/DPP4 in organ fibrosis
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  • Wolfgang Jungraithmayr,
  • Isabelle Moneke,
  • Birte Ohm,
  • Ingrid De Meester
Wolfgang Jungraithmayr
University Hospital Freiburg

Corresponding Author:[email protected]

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Isabelle Moneke
University Medical Center Freiburg
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Birte Ohm
University Medical Center Freiburg
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Ingrid De Meester
Universiteit Antwerpen Faculteit Farmaceutische Biomedische en Diergeneeskundige Wetenschappen
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Abstract

CD26/DPP4 is an exopeptidase that is expressed on the cell surface of many organs but is also present in a circulating soluble form. Beyond its enzymatic and co-stimulatory activity, CD26/DPP4 is involved in the pathogenesis of chronic fibrosis across many organ diseases such as liver cirrhosis, kidney failure, and lung fibrosis, but CD26/DPP4 has also impact on the epithelial-to-mesenchymal transition (EMT) pathway during cancer formation, chronic transplant rejection and autoimmune diseases. The morbidity and mortality caused by fibrotic disorders is high, and no effective therapies are available. Growing evidence suggests that the inhibition of CD26/DPP4 can attenuate the progress of fibrotic diseases via modulating the EMT milieu and other pathways. This review summarizes the role of CD26/DPP4 in fibrosis-associated diseases and highlight new opportunities of how CD26/DPP4-inhibitors may reduce or reverse fibrosis. As a major advantage, CD26/DPP4-inhibitors are in safe and routine clinical use against type 2 diabetes for many years with few side effects making them promising therapeutics for a novel clinical application in fibrotic disorders.