Martins_2024_Am.J.Physiol.Cell.Physiol_326_C1203

Reference

Title : Bidirectional relation between dipeptidyl peptidase 4 and angiotensin II type I receptor signaling - Martins_2024_Am.J.Physiol.Cell.Physiol_326_C1203
Author(s) : Martins FL , Ribeiro-Silva JC , Nistala R , Girardi ACC
Ref : American Journal of Physiology Cell Physiol , 326 :C1203 , 2024
Abstract : Cardiometabolic diseases are often associated with heightened levels of angiotensin II (Ang II), which accounts for the observed oxidative stress, inflammation, and fibrosis. Accumulating evidence indicates a parallel upregulation of dipeptidyl dipeptidase 4 (DPP4) activity in cardiometabolic diseases, with its inhibition shown to mitigate oxidative stress, inflammation, and fibrosis. These findings highlight an overlap between the pathophysiological mechanisms used by Ang II and DPP4. Recent evidence demonstrates that targeted inhibition of DPP4 prevents the rise in Ang II and its associated molecules in experimental models of cardiometabolic diseases. Similarly, inhibitors of the angiotensin I-converting enzyme (ACE) or Ang II type 1 receptor (AT1R) blockers downregulate DPP4 activity, establishing a bidirectional relationship between DPP4 and Ang II. Here, we discuss the current evidence supporting the cross talk between Ang II and DPP4, along with the potential mechanisms promoting this cross regulation. A comprehensive analysis of this bidirectional relationship across tissues will advance our understanding of how DPP4 and Ang II collectively promote the development and progression of cardiometabolic diseases.
ESTHER : Martins_2024_Am.J.Physiol.Cell.Physiol_326_C1203
PubMedSearch : Martins_2024_Am.J.Physiol.Cell.Physiol_326_C1203
PubMedID: 38581656

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Citations formats

Martins FL, Ribeiro-Silva JC, Nistala R, Girardi ACC (2024)
Bidirectional relation between dipeptidyl peptidase 4 and angiotensin II type I receptor signaling
American Journal of Physiology Cell Physiol 326 :C1203

Martins FL, Ribeiro-Silva JC, Nistala R, Girardi ACC (2024)
American Journal of Physiology Cell Physiol 326 :C1203