The drug-treated mice had almost half as many dying cells in their artery plaques, which could mean their plaques are less damaged and more stable.

Scientific Claim

Treatment with MPE-298 in apolipoprotein E-deficient mice on a high-fat high-cholesterol diet is associated with a 45% reduction in caspase-3-positive cells in brachiocephalic artery lesions, suggesting a link to decreased apoptosis in atherosclerotic plaques.

Original Statement

“In mice treated with MPE-298, immunostained caspase-3 was reduced by 45% (p < 0.01) compared to that in vehicle-treated animals (Figure 3B).”

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 claim implies MPE-298 causes reduced apoptosis, but the study design cannot establish causation; only association is supported.

More Accurate Statement

“Treatment with MPE-298 in apolipoprotein E-deficient mice on a high-fat high-cholesterol diet is associated with a 45% reduction in caspase-3-positive cells in brachiocephalic artery lesions.”

Evidence from Studies

Supporting (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 found that a drug called MPE-298 helps make dangerous artery plaques more stable in mice, which likely means fewer cells in the plaques are dying—exactly what the claim says.

Contradicting (0)

No contradicting evidence found

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

There was a hint that the drug might help turn some immune cells into a less inflammatory type, but the data weren’t strong enough to be sure.

86%

The drug seemed to make more of the CD36 protein visible in the artery plaques, which might help the body clear dead cells better.

86%

The drug didn’t make the fibrous cap around the plaque thicker, so its protective effect must come from other changes, like less cell death or inflammation.

83%

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.

79%

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.

79%