Key result
Nrf2 deficiency extends survival by ~20 weeks and prevents hypertrophy in protein aggregation cardiomyopathy.
Why the study?
Sustained activation of Nrf2 causes reductive stress contributing to proteotoxic cardiac disease, but whether disrupting Nrf2 signaling prevents this was unknown.
Does Nrf2 deficiency prevent reductive stress-induced hypertrophic cardiomyopathy in a transgenic mouse model?
Population
Non-transgenic, transgenic MPAC, and MPAC-TG:Nrf2-deficient mice
Comparison
Nrf2 deficiency vs Nrf2 intact in transgenic MPAC mice
Design
Preclinical study
Follow-up
Up to 60 weeks
Authors
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Nrf2 deficiency may protect against reductive stress cardiomyopathy in mice; leaves open therapeutic relevance in human proteotoxic heart disease.
Does Nrf2 deficiency prevent reductive stress-induced hypertrophic cardiomyopathy in a transgenic mouse model?
Nrf2 deficiency prevents reductive stress and mutant protein aggregation, thereby delaying proteotoxic cardiac remodeling and heart failure in a mouse model.
Kannan et al. (2013) studied Mutant protein aggregation cardiomyopathy. Nrf2 deficiency vs. Transgenic mice with intact Nrf2 was evaluated on Survival, cardiac hypertrophy, and protein aggregation. Nrf2 deficiency prevented reductive stress, prolonged survival by 20-25 weeks, and prevented cardiac hypertrophy up to 60 weeks in transgenic mice with mutant protein aggregation cardiomyopathy.
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