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Published on: June 7, 2016
Emerging Role of Angiotensin AT2 Receptor in Anti-Inflammation: An Update
Sanket N Patel1, Naureen Fatima1, Riyasat Ali1
1Department of Pharmacological & Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, United States.
Abstract:
The hyperactive RAS and inflammation are closely associated. The angiotensin-II/AT1R axis of the RAS has been explored extensively for its role in inflammation and a plethora of pathological conditions. Understanding the role of AT2R in inflammation is an emerging area of research. The AT2R is expressed on a variety of immune and non-immune cells, which upon activation triggers the release of a host of cytokines and has multiple effects that coalesce to anti-inflammation and prevents maladaptive repair. The anti-inflammatory outcomes of AT2R activation are linked to its well-established signaling pathways involving formation of nitric oxide and activation of phosphatases. Collectively, these effects promote cell survival and tissue function. The consideration of AT2R as a therapeutic target requires further investigations.
Insights
The angiotensin II type 2 receptor (AT2R) shows anti-inflammatory effects by releasing cytokines and promoting tissue repair. Further research is needed to explore AT2R as a potential therapeutic target for inflammatory conditions.
Area of Science:
- Immunology
- Cardiovascular Research
- Pharmacology
Background:
- The Renin-Angiotensin System (RAS) plays a key role in inflammation, with the angiotensin II/AT1 receptor (AT1R) axis extensively studied.
- The role of the angiotensin II type 2 receptor (AT2R) in inflammation is an emerging area of significant research interest.
Purpose of the Study:
- To elucidate the emerging role of AT2R in modulating inflammatory responses.
- To explore the potential of AT2R as a therapeutic target.
Main Methods:
- Review of existing literature on AT2R expression and function in immune and non-immune cells.
- Analysis of signaling pathways downstream of AT2R activation, including nitric oxide formation and phosphatase activity.
Main Results:
- AT2R is expressed on various cell types and its activation triggers cytokine release.
- AT2R activation demonstrates anti-inflammatory effects and prevents maladaptive tissue repair.
- Signaling pathways involving nitric oxide and phosphatases are linked to AT2R's anti-inflammatory outcomes.
Conclusions:
- AT2R activation promotes cell survival and tissue function through anti-inflammatory mechanisms.
- The findings highlight the potential of AT2R as a novel therapeutic target for inflammatory diseases.
- Further investigation into AT2R's therapeutic potential is warranted.
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