The drug lowered the levels of two proteins in the arteries that are known to break down plaque structure, which might help keep plaques from bursting.

Scientific Claim

In apolipoprotein E-deficient mice on a high-fat high-cholesterol diet, MPE-298 treatment is associated with a 56% reduction in Mmp14 mRNA levels and a 44% reduction in Plau mRNA levels in abdominal aorta tissue, suggesting a link to decreased expression of plaque-destabilizing enzymes.

Original Statement

“In mice treated with cyclic azapeptide MPE-298, mRNA levels of Plat, Plau, and Mmp14 were reduced by 63% (p < 0.05), 44% (p < 0.001), and 56% (p < 0.05), respectively, compared to those in vehicle-treated animals (Figure 4A).”

From study:A cyclic azapeptide ligand of the scavenger receptor CD36/SR-B2 reduces the atherosclerotic lesion progression and enhances plaque stability in apolipoprotein E-deficient mice

Evidence Quality Assessment

Claim Status

overstated

Study Design Support

Design supports claim

Appropriate Language Strength

association

Can only show association/correlation

Assessment Explanation

The authors imply causation ('reduced'), but the study design (animal model, no human translation) only permits association claims.

More Accurate Statement

“In apolipoprotein E-deficient mice on a high-fat high-cholesterol diet, MPE-298 treatment is associated with a 56% reduction in Mmp14 mRNA levels and a 44% reduction in Plau mRNA levels in abdominal aorta tissue.”

Evidence from Studies

Supporting (0)

No supporting evidence found

Contradicting (1)

A cyclic azapeptide ligand of the scavenger receptor CD36/SR-B2 reduces the atherosclerotic lesion progression and enhances plaque stability in apolipoprotein E-deficient mice

Randomized Controlled Trial

Animal

2023

The study says a drug called MPE-298 helps stabilize dangerous plaques in mice, but it never measured the specific genes mentioned in the claim, so we can't say if those gene changes really happened.

Source Study

A cyclic azapeptide ligand of the scavenger receptor CD36/SR-B2 reduces the atherosclerotic lesion progression and enhances plaque stability in apolipoprotein E-deficient mice

Score: 12

DOI: 10.3389/fphar.2023.1204905

Similar Assertions

Mice treated with the drug had much smaller dead-cell areas in their artery plaques—almost half as big—which might mean their plaques are less likely to break open.

82%

The drug didn’t lower the mice’s overall cholesterol, so its benefits must come from something else—like reducing inflammation or cell death in plaques.

81%

The drug lowered two key inflammation signals in the blood by nearly half, which may help calm down the body’s harmful immune response in the arteries.

79%

The drug didn’t affect blood sugar or fat levels in the blood, so its benefits aren’t due to improving how the body handles sugar or fat.

79%

The mice didn’t gain or lose weight or eat differently with the drug, so the benefits aren’t just because they were eating less or changing their metabolism.

78%