Nε-carboxyethyl-lysin influences atherosclerotic plaque stability through ZKSCAN3 acetylation-regulated macrophage autophagy via the RAGE/Liver Kinase B1 (LKB1)/AMPK1/SIRT1 pathway
Authors' conclusion
These findings highlight CEL's critical role in promoting plaque instability in T2DM by impairing key molecular pathways that regulate autophagy
Study context
- Population
- Patients with coronary artery disease; murine model of atherosclerosis complicated by T2DMCAD cohort
- Participants
- 225 patients
Methodological detailsclinical cohort, murine model of atherosclerosis complicated by T2DM, metabolomic profiling
- Clinical cohort
- Murine model of atherosclerosis complicated by T2DM
- Metabolomic profiling
Main finding
As reported in the abstract
- Elevated serum CEL levels independently associated with increased acute coronary syndrome (ACS) incidence
- Metabolomic profiling identified CEL as a key AGE contributing to plaque instability in diabetic conditions
- CEL disrupted macrophage autophagy and plaque stability by perturbing the RAGE/LKB1/AMPK1/SIRT1 signaling cascade
- This pathway regulated autophagic activity through SIRT1-mediated acetylation of ZKSCAN3
Original publication
Nε-carboxyethyl-lysin influences atherosclerotic plaque stability through ZKSCAN3 acetylation-regulated macrophage autophagy via the RAGE/LKB1/AMPK1/SIRT1 pathway. Cardiovasc Diabetol. Published 22 January 2025. doi:10.
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