Key result
Skeletal muscle knockout of Nox4 provided full protection against loss of diaphragm maximal force in HFrEF mice (p<0.01), while Nox2 knockout provided partial protection (7% depression, p<0.01).
Why the study?
Diaphragm weakness in HFrEF is linked to excessive reactive oxygen species, but the exact source of ROS and the role of skeletal muscle Nox2 and Nox4 remain unknown.
Does skeletal muscle specific knockout of Nox2 or Nox4 prevent loss of maximal diaphragm force in a mouse model of HFrEF?
Population
Mouse model of HFrEF induced by myocardial infarction
Comparison
Inducible skeletal muscle-specific knockout of Nox2 or Nox4 vs controls
Design
Preclinical animal study using the Cre-Lox system
Authors
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Nox4 may mediate diaphragm weakness in experimental HFrEF; leaves open translation to human therapies.
Does skeletal muscle specific knockout of Nox2 or Nox4 prevent loss of maximal diaphragm force in a mouse model of HFrEF?
p-value: p=<0.01
Skeletal muscle Nox4 and Nox2 contribute to diaphragm weakness in HFrEF, and their targeted knockout preserves diaphragm force and improves survival in a mouse model.
Kumar et al. (2022) studied Heart failure with reduced ejection fraction (HFrEF). Skeletal muscle specific knockouts of Nox2 or Nox4 vs. Control mice with HFrEF was evaluated on Diaphragm maximal specific force (p=<0.01). Skeletal muscle knockout of Nox4 provided full protection against loss of diaphragm maximal force in HFrEF mice (p<0.01), while Nox2 knockout provided partial protection (7% depression, p<0.01).