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The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
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Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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Renin-angiotensin system and inflammation update.

Elena Cantero-Navarro1, Beatriz Fernández-Fernández2, Adrian M Ramos2

  • 1Molecular and Cellular Biology in Renal and Vascular Pathology. IIS-Fundación Jiménez Díaz-Universidad Autónoma, Madrid, Spain; Red de Investigación Renal (REDINREN), Spain.

Molecular and Cellular Endocrinology
|April 2, 2021
PubMed
Summary

The renin-angiotensin system (RAS) plays a dual role in inflammation, with Angiotensin II (Ang II) promoting damage via AT1R, while other RAS components like ACE2 and AT2R may offer protective anti-inflammatory effects. Novel research explores intracellular receptors, epigenetic regulation, and the downregulation of key anti-inflammatory factors.

Keywords:
Ac-SDKPAngiotensinInflammationKidneyKlothoPGC-1αTh17miRNA

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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • The classical view of the renin-angiotensin system (RAS) focuses on blood pressure and sodium balance.
  • Emerging evidence highlights the RAS's significant role in modulating inflammation and contributing to organ damage.
  • Angiotensin II (Ang II) acting through angiotensin type 1 receptors (AT1R) promotes inflammation, forming the basis for RAS blocker therapies.

Purpose of the Study:

  • To review recent advances in understanding the complex interactions between the RAS and inflammatory processes.
  • To highlight novel insights into RAS components that may exert anti-inflammatory effects.
  • To discuss the mechanisms by which the RAS downregulates crucial anti-inflammatory factors.

Main Methods:

  • Literature review of recent scientific advances in RAS and inflammation research.
  • Analysis of novel findings concerning intracellular angiotensin receptors.
  • Examination of RAS interactions with immune cells, receptors (TLRs), and epigenetic regulators (miRNAs, BET proteins).

Main Results:

  • The RAS exhibits pleiotropic effects on inflammation, with both pro- and anti-inflammatory pathways.
  • Angiotensin-converting enzyme 2 (ACE2) and Angiotensin type 2 receptor (AT2R) activation show potential for anti-inflammatory responses.
  • Novel insights include the role of intracellular receptors, AT1R modifications, immune cell modulation, and epigenetic regulation in RAS-mediated inflammation.
  • The RAS actively downregulates key anti-inflammatory factors like klotho, PGC-1α, and Ac-SDKP through transcription factors and epigenetic mechanisms.

Conclusions:

  • The RAS is a critical regulator of inflammation with complex, context-dependent effects.
  • Targeting specific RAS components and pathways offers potential therapeutic strategies for inflammatory diseases.
  • Further research into the intricate mechanisms of RAS-mediated inflammation, particularly the downregulation of anti-inflammatory factors, is warranted.