Even though the mice had fatty plaques and they burst, their blood fat levels didn’t change — meaning the rupture wasn’t caused by worse cholesterol, but by something else, like immune activity.

Scientific Claim

In apolipoprotein E-knockout mice, short-term combination stimulation does not alter serum levels of total cholesterol, triglycerides, LDL, or HDL at 6 or 14 weeks, indicating that plaque rupture in this model is independent of systemic lipid changes.

Original Statement

“However, the control and treatment groups did not differ with respect to the serum lipid levels at 6 or 14 weeks (Table 1).”

From study:Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout 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 study reports null findings with precise data and statistical analysis. The conclusion that lipid levels are unchanged is appropriately stated and supports the study’s focus on immune mechanisms.

Evidence from Studies

Supporting (1)

Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Cohort Study

Animal

2013 Jul

Even though the mice didn’t have higher cholesterol or fat levels in their blood, they still got dangerous plaque bursts — and that was caused by immune system activity, not fats.

Contradicting (0)

No contradicting evidence found

Source Study

Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Score: 17

DOI: 10.1038/cmi.2013.4

Similar Assertions

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