Key result
Chronic reductive stress increases the myocardial TEI index up to ~4-fold, inducing severe dyssynchrony in mice.
Population
Cardiac-specific constitutively active Nrf2 transgenic and NTG mice at ~3 and 6 months of age
Comparison
Cardiac-specific constitutively active Nrf2… vs Non-transgenic (NTG) mice
Design
Preclinical
Follow-up
up to 6 months of age
Authors
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Chronic reductive stress driven by constitutively active Nrf2 induces non-amyloid proteotoxicity and cardiac dyssynchrony in mice, challenging the assumption that antioxidants are universally beneficial.
Effect estimate: 2 and 4-fold increase
p-value: p=>0.0001
Chronic reductive stress driven by constitutively active Nrf2 induces non-amyloid proteotoxicity and cardiac dyssynchrony in mice, challenging the assumption that antioxidants are universally beneficial.
Sunny et al. (2025) studied Chronic reductive stress-induced cardiac remodeling and dyskinesia. Chronic reductive stress (CaNrf2-TGL/TGH transgenic model) vs. Non-transgenic (NTG) mice was evaluated on TEI index (measure of global cardiac function) (2 and 4-fold increase, p=>0.0001). Chronic reductive stress in transgenic mice significantly elevated the TEI index by 2- to 4-fold (P>0.0001) and induced severe segmental dyssynchrony compared to non-transgenic mice at 6 months.
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