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The biology of the (pro)renin receptor

Genevieve Nguyen1, Dominik N Muller

  • 1Institut de la Santé et de la Recherche Médicale, Collège de France, Paris, France. genevieve.nguyen@college-de-france.fr

Journal of the American Society of Nephrology : JASN
|November 18, 2009
PubMed

Insights

The (pro)renin receptor (PRR) activates prorenin, potentially causing organ damage in hypertension and diabetes. Further research is needed to confirm PRR's role in disease and explore therapeutic strategies.

Area of Science:

  • Biochemistry
  • Physiology
  • Pathology

Background:

  • The (pro)renin receptor (PRR) binds renin and prorenin, activating prorenin to an enzymatically active form.
  • PRR activation triggers MAP kinases (ERK1/2, p38) and upregulates profibrotic and cyclooxygenase-2 genes, independent of angiotensin II.
  • PRR's role in organ damage in hypertension and diabetes is of significant interest due to its connection with the renin-angiotensin system (RAS).

Purpose of the Study:

  • To elucidate the physiological and pathological roles of the (pro)renin receptor (PRR).
  • To investigate the contribution of PRR to organ damage in diseases like hypertension and diabetes.
  • To assess the potential of targeting PRR for therapeutic interventions.

Main Methods:

  • Review of existing literature on PRR function and its involvement in disease models.
  • Analysis of data from transgenic animal models overexpressing PRR.
  • Consideration of studies involving PRR-null mice and PRR antagonists.

Main Results:

  • Overexpression of PRR in transgenic animals leads to hypertension and glomerulosclerosis.
  • Increased PRR expression is observed in models of hypertension and kidney damage.
  • PRR-null mice exhibit early embryonic lethality, indicating essential cellular functions.

Conclusions:

  • While PRR's identification advanced understanding of tissue RAS physiology, its precise role in pathology remains unclear.
  • Definitive proof for PRR's role in disease requires further investigation, such as tissue-specific ablation or antagonist studies.
  • PRR possesses essential cellular functions beyond its role in the RAS, as evidenced by embryonic lethality in knockout models.

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