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

Scientific Claim

In apolipoprotein E-deficient mice on a high-fat high-cholesterol diet, MPE-298 treatment is associated with increased CD36 immunofluorescence in brachiocephalic artery lesions compared to vehicle-treated mice, suggesting a potential modulation of CD36 expression or retention in plaques.

Original Statement

“On the contrary, animals treated with azapeptides tended to exhibit increased CD36 staining in lesion areas compared to that in the vehicle-treated mice (Figure 2D).”

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 a definitive effect ('increased'), but the data are described as a 'tendency' without statistical significance, warranting cautious association language.

More Accurate Statement

“In apolipoprotein E-deficient mice on a high-fat high-cholesterol diet, MPE-298 treatment is associated with a trend toward increased CD36 immunofluorescence in brachiocephalic artery lesions compared to vehicle-treated mice.”

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 reduce dangerous plaques in mice, and it works by interacting with a protein called CD36—but it never measured whether CD36 increased in the plaques, so we can't say it did.

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.

89%

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.

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.

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.

78%

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.

76%