Key result
In a mouse model of pressure overload, administration of the Nrf2 activator dh404 dose-dependently inhibited pathological cardiac remodeling and dysfunction, and reduced mortality.
Why the study?
Does the Nrf2 activator dh404 prevent pathological cardiac remodeling and dysfunction in mice subjected to hemodynamic stress?
Population
Male C57BL/6J mice subjected to transverse aortic constriction to induce cardiac maladaptive remodeling and…
Comparison
Dihydro-CDDO-trifluoroethylamide administered by… vs Vehicle in sham or TAC operated mice. In vitro…
Design
Preclinical
Follow-up
4 weeks
Authors
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Should not change clinical practice; leaves open Nrf2 activation as a target for human heart failure.
Does the Nrf2 activator dh404 prevent pathological cardiac remodeling and dysfunction in mice subjected to hemodynamic stress?
p-value: p=<0.05
The Nrf2 activator dh404 prevents pathological cardiac remodeling and dysfunction in a mouse model of pressure overload, highlighting Nrf2 as a potential therapeutic target for heart failure.
Xing et al. (2012) studied Pathological cardiac remodeling and heart failure. Dihydro-CDDO-trifluoroethyl amide (dh404) vs. Vehicle (sesame oil) was evaluated on Cardiac remodeling and dysfunction (e.g., fractional shortening, hypertrophy) (p=<0.05). In a mouse model of pressure overload, administration of the Nrf2 activator dh404 dose-dependently inhibited pathological cardiac remodeling and dysfunction, and reduced mortality.
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