Key result
Treatment of obstructed kidneys with Arid2-IR shRNA blunted NF-κB-driven renal inflammation without affecting TGF-β/Smad3-mediated renal fibrosis.
Why the study?
Does Arid2-IR knockdown reduce renal inflammation in a mouse model of obstructive nephropathy?
Population
Smad3 wild-type and knockout mice with induced obstructive nephropathy, and in vitro tubular epithelial cells
Comparison
Knockdown or overexpression of Arid2-IR vs Control (untreated or wild-type/control vector)
Design
Preclinical
Authors
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Arid2-IR knockdown selectively targets renal inflammation in preclinical models; leaves open therapeutic translation pending human studies.
Does Arid2-IR knockdown reduce renal inflammation in a mouse model of obstructive nephropathy?
Arid2-IR is a Smad3-associated lncRNA that promotes NF-κB-dependent renal inflammation, and its blockade may serve as a novel therapeutic target for renal inflammatory disease.
Zhou et al. (2015) studied Renal inflammation and fibrosis. Arid2-IR shRNA was evaluated on NF-κB-driven renal inflammation and TGF-β/Smad3-mediated renal fibrosis. Treatment of obstructed kidneys with Arid2-IR shRNA blunted NF-κB-driven renal inflammation without affecting TGF-β/Smad3-mediated renal fibrosis.
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