Increased cyclooxygenase-2, hyperfiltration, glomerulosclerosis, and diabetic nephropathy: put the blame on the (pro)renin receptor?
Interaction between the renin-angiotensin system and cyclooxygenases in the kidney regulates renal microcirculation. Activation of the (pro)renin receptor has profibrotic effects, and now Kaneshiroet al. show that it also increases COX-2 synthesis. These results may have therapeutic implications, as blocking (pro)renin-receptor interaction would prevent the increase of angiotensin generation and prostaglandin synthesis, two phenomena underlying the pathogenesis of diabetic nephropathy.
Nguyen
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Institut National de la Santé et de la Recherche Médicale, Unit 36, Collège de France, Unit of Experimental Medicine, Paris, France. genevieve.nguyen@college-de-france.fr
D000818:Animals; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism*; D003928:Diabetic Nephropathies / Q000378:metabolism / Q000503:physiopathology*; D005786:Gene Expression Regulation; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000098:blood supply / Q000378:metabolism; D008833:Microcirculation / Q000502:physiology; D051381:Rats; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000502:physiology; D000093342:Prorenin Receptor
D011956:Receptors, Cell Surface; D051546:Cyclooxygenase 2; D000093342:Prorenin Receptor