In people having a heart attack, PLIN2 protein stays high even though the cellular cleanup system (proteasome) is more active, suggesting there might be special reasons why PLIN2 isn't being broken down properly during a heart attack.

Scientific Claim

In ST-elevation myocardial infarction (STEMI) patients, perilipin-2 (PLIN2) protein levels remain elevated despite higher proteasome activity, suggesting potential mechanisms for PLIN2 escape from proteasomal degradation in acute coronary events.

Original Statement

“Despite the proteasome activity being higher in STEMI patients, probably due to the elevated inflammatory burden, PLIN2 could escape proteasome degradation in a more efficient manner in STEMI as compared to CCS patients.”

From study:Regulation of Monocyte Perilipin-2 Expression in Acute and Chronic Coronary Syndromes: Pathogenetic Implications

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 is observational and reports a potential disconnect between proteasome activity and PLIN2 levels. The claim uses 'suggesting potential mechanisms' which appropriately reflects the observational nature of the study and avoids causal language.

Evidence from Studies

Supporting (1)

Regulation of Monocyte Perilipin-2 Expression in Acute and Chronic Coronary Syndromes: Pathogenetic Implications

Cross-Sectional Study

Human

Contradicting (0)

No contradicting evidence found

Source Study

Regulation of Monocyte Perilipin-2 Expression in Acute and Chronic Coronary Syndromes: Pathogenetic Implications

Score: 37

DOI: 10.3390/ijms26199550

Similar Assertions

In people with stable heart disease, when the proteasome (cellular cleanup system) is more active, there's less PLIN2 protein present, but this relationship doesn't hold for people having a heart attack, suggesting different ways PLIN2 is regulated in these two conditions.

90%

In people with stable heart disease, when the proteasome (a cellular cleanup system) is more active, there's less PLIN2 protein present, but this relationship doesn't hold for people having a heart attack.

88%

In people having a heart attack called STEMI, the amount of a protein called PLIN2 in certain blood cells is higher than in people with stable heart disease, which might be related to why their heart attack happened.

83%

In people with heart disease, older patients tend to have higher levels of PLIN2 protein in their blood cells, and this relationship is stronger in those with stable heart disease than in those having a heart attack.

81%

In people with stable heart disease, older age is more strongly linked to higher PLIN2 protein levels than in people having a heart attack, suggesting age might affect PLIN2 differently in different types of heart disease.

78%