Key result
Silencing of the nAChR α1 gene in a mouse model of obstructive uropathy reduced fibrosis severity by 24% and significantly decreased interstitial myofibroblasts, indicating that a uPA-dependent nAChR α1 pathway promotes renal fibrosis.
Population
Mouse obstructive uropathy model of chronic kidney disease in wild-type C57BL/6 and uPA-/- C57BL/6 mice, and…
Comparison
Silencing of the nAChRalpha1 gene and uPA… vs Scrambled siRNA (pscr) or unstimulated controls
Design
Preclinical
Follow-up
7 days (in vivo UUO model)
Authors
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Hypothesis-generating for nAChR α1 inhibition in renal fibrosis; leaves open translation to human disease.
Effect estimate: 24% decrease
p-value: p=<0.05
nAChRalpha1 acts as a uPA signaling receptor that promotes renal fibrosis, suggesting a novel therapeutic target for fibrotic diseases.
Zhang et al. (2009) studied Renal fibrosis. nAChR α1 gene silencing (psir2 plasmid) vs. Scrambled RNA plasmid (pscr) was evaluated on Fibrosis severity (total collagen) (24% decrease, p=<0.05). Silencing of the nAChR α1 gene in a mouse model of obstructive uropathy reduced fibrosis severity by 24% and significantly decreased interstitial myofibroblasts, indicating that a uPA-dependent nAChR α1 pathway promotes renal fibrosis.
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