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.

Scientific Claim

In apolipoprotein E-deficient mice on a high-fat high-cholesterol diet, MPE-298 treatment is associated with no significant change in collagen content within brachiocephalic artery lesions compared to vehicle controls, suggesting that plaque stability improvements are not due to increased fibrous cap thickness.

Original Statement

“Collagen-stained areas did not reveal significant differences between the two groups (Figure 3C).”

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

appropriately stated

Study Design Support

Design supports claim

Appropriate Language Strength

association

Can only show association/correlation

Assessment Explanation

The claim correctly uses neutral language and accurately reflects the non-significant finding, consistent with study design limitations.

More Accurate Statement

“In apolipoprotein E-deficient mice on a high-fat high-cholesterol diet, MPE-298 treatment is associated with no significant change in collagen content within brachiocephalic artery lesions compared to vehicle controls.”

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 the drug makes plaques more stable, but it never measured the collagen in the plaque’s protective cap, so we can’t tell if the cap got thicker or not.

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

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.

83%

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

82%

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.

80%

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.

80%

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%