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Bidirectional relation between dipeptidyl peptidase 4 and angiotensin II type I receptor signaling.

Authors :
Martins FL
Ribeiro-Silva JC
Nistala R
Girardi ACC
Source :
American journal of physiology. Cell physiology [Am J Physiol Cell Physiol] 2024 Apr 01; Vol. 326 (4), pp. C1203-C1211. Date of Electronic Publication: 2024 Mar 04.
Publication Year :
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.

Details

Language :
English
ISSN :
1522-1563
Volume :
326
Issue :
4
Database :
MEDLINE
Journal :
American journal of physiology. Cell physiology
Publication Type :
Academic Journal
Accession number :
38581656
Full Text :
https://doi.org/10.1152/ajpcell.00734.2023