Key result
Wild-type mice reconstituted with bone marrow lacking the angiotensin II type 1 receptor developed significantly more severe renal interstitial fibrosis 14 days after ureteral obstruction compared to controls.
Why the study?
Does the absence of Agtr1 on bone marrow-derived macrophages worsen renal fibrosis in a mouse model of unilateral ureteral obstruction?
Does the absence of Agtr1 on bone marrow-derived macrophages worsen renal fibrosis in a mouse model of unilateral ureteral obstruction?
Absolute Event Rate: 139% vs 93%
p-value: p=<0.005
The absence of the angiotensin II type 1 receptor on bone marrow-derived macrophages exacerbates renal fibrosis during urinary tract obstruction, likely due to impaired macrophage phagocytic capability.
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Macrophage AT1 signaling may limit obstructive renal fibrosis; hypothesis-generating for human CKD with no immediate clinical implications.
Nishida et al. (2002) studied Renal fibrosis (n=37). Agtr1-/- bone marrow transplantation vs. Agtr1+/+ bone marrow transplantation was evaluated on Interstitial collagen fractional volume (points per 1000) at 14 days after unilateral ureteral obstruction (p=<0.005). Wild-type mice reconstituted with bone marrow lacking the angiotensin II type 1 receptor developed significantly more severe renal interstitial fibrosis 14 days after ureteral obstruction compared to controls.
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