Key result
High glucose exposure in rat mesangial cells up-regulates the (pro)renin receptor, leading to increased production of inflammatory factors IL-1β and COX-2 via an angiotensin II-dependent pathway.
Why the study?
Does high glucose induce IL-1beta and COX-2 production via enhanced (pro)renin receptor expression in rat mesangial cells?
Does high glucose induce IL-1beta and COX-2 production via enhanced (pro)renin receptor expression in rat mesangial cells?
This study demonstrates that high glucose induces renal inflammation by up-regulating the (pro)renin receptor, leading to increased IL-1beta and COX-2 production via angiotensin II-dependent and ERK1/2-NF-kappaB pathways.
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May implicate (pro)renin receptor in diabetic renal inflammation; leaves open clinical translation and therapeutic targeting.
Huang et al. (2009) studied Hyperglycemia / Diabetic Nephropathy (In vitro model). High D-glucose vs. L-glucose (control) was evaluated on Expression of (pro)renin receptor (PRR), IL-1β, and COX-2. High glucose exposure in rat mesangial cells up-regulates the (pro)renin receptor, leading to increased production of inflammatory factors IL-1β and COX-2 via an angiotensin II-dependent pathway.
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