[HTML][HTML] Increased cyclooxygenase-2, hyperfiltration, glomerulosclerosis, and diabetic nephropathy: put the blame on the (pro) renin receptor?
G Nguyen - Kidney international, 2006 - Elsevier
G Nguyen
Kidney international, 2006•ElsevierInteraction 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.
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.
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.
Elsevier