Key result
AT1A receptor deficiency in MRL-Faslpr/lpr mice significantly reduced mean survival from 162 to 117 days and accelerated kidney injury due to activation of glomerular AT1B receptors.
Why the study?
Does AT1A receptor deficiency protect against autoimmune nephritis in MRL-Faslpr/lpr mice?
Population
MRL-Faslpr/lpr mice lacking the major murine type 1 angiotensin receptor and wild-type lpr controls.
Comparison
Genetic deletion of AT1A receptors; subsets… vs MRL-Faslpr/lpr mice with intact AT1A receptors.
Design
Preclinical
Follow-up
up to 234 days
Authors
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AT1A deficiency worsens outcomes in this murine nephritis model; challenges presumed protective effects and leaves open AT1B compensation for targeted study.
Does AT1A receptor deficiency protect against autoimmune nephritis in MRL-Faslpr/lpr mice?
Absolute Event Rate: 117% vs 162%
p-value: p=0.001
In a murine model of autoimmune nephritis, AT1A receptor deficiency paradoxically accelerated renal injury and mortality due to compensatory activation of glomerular AT1B receptors.
Crowley et al. (2009) studied Autoimmune nephritis (SLE model) (n=85). AT1A receptor deficiency vs. Wild-type AT1A (lpr controls) was evaluated on Mean duration of survival (days) (p=0.001). AT1A receptor deficiency in MRL-Faslpr/lpr mice significantly reduced mean survival from 162 to 117 days and accelerated kidney injury due to activation of glomerular AT1B receptors.
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