Mice with a specific genetic modification that causes heart failure had more than double the oxidative stress in their heart cells compared to normal mice.
Scientific Claim
Cardiac-specific MST-1 overexpression in mice resulted in 119% greater cardiac oxidative stress compared to wild-type mice.
Original Statement
“Cardiac oxidative stress was 119% greater in MST‐1 than in wild type (P < 0.001)”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The claim correctly describes the comparison between mouse groups without implying causation beyond the study design. It specifies the model and measurement method.
More Accurate Statement
“Cardiac-specific MST-1 overexpression in mice was associated with 119% greater cardiac oxidative stress compared to wild-type mice.”
Evidence from Studies
Supporting (1)
N‐acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure